3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11965&form=6&db=m Properties of rat kidney glutaminase enzymes and their role in renal ammoniagenesis. causal interaction,ongoing research,unassigned 1,3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12662&form=6&db=m Effect of pH on ammonia production by renal mitochondria. causal interaction,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18540&form=6&db=m Biochemical and histocytochemical studies on response of ammonia-producing enzymes for nh4cl-induced acidosis. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=127007&form=6&db=m Effects of age on renal function and enzyme activity in male C57BL/6 mice. diagnostic usage,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=185045&form=6&db=m Acidosis activation of the pituitary-adrenal-renal glutaminase I axis. therapeutic application,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=234956&form=6&db=m Phosphate-independent glutaminase from rat kidney. Partial purification and identity with gamma-glutamyltranspeptidase. ongoing research,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=461451&form=6&db=m Renal phosphate-dependent glutaminase activity and ammonia excretion during acute acidosis in the rat. ongoing research,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=616362&form=6&db=m A comparative study of the renal glutaminase response to acidosis. ongoing research,therapeutic application,unassigned 4,2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=631264&form=6&db=m A lack of correlation between rat kidney mitochondrial swelling and glutaminase activation in metabolic acidosis. ongoing research,unassigned 2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1001010&form=6&db=m Phosphate activation of glutaminase in sonicated mitochondria of normal and acidotic rat kidneys. ongoing research,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1252072&form=6&db=m Phosphate-dependent glutaminase from rat kidney. Cause of increased activity in response to acidosis and identity with glutaminase from other tissues. ongoing research,unassigned 2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1265082&form=6&db=m Ammonia formation from glutamine isomers by nonacidotic and acidotic perfused rat kidneys. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1709637&form=6&db=m Effect of acute alterations in acid-base balance on rat renal glutaminase and phosphoenolpyruvate carboxykinase gene expression. causal interaction,unassigned 2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1756643&form=6&db=m Effect of acidosis on phosphoenolpyruvate carboxykinase and glutaminase mRNAs in rat kidney and in LLC-PK-F+ cells. ongoing research,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1770913&form=6&db=m Adaptation of renal tricarboxylic acid cycle metabolism to various acid-base states: study with [3-13C,5-15N]glutamine. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1779958&form=6&db=m Variations in the kinetic response of several different phosphate-dependent glutaminase isozymes during acute metabolic acidosis. ongoing research,therapeutic application,unassigned 3,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1854751&form=6&db=m Mechanism of altered renal glutaminase gene expression in response to chronic acidosis. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1887909&form=6&db=m Pathways of acute pH regulation of ammoniagenesis in LLC-PK1 cells: study with [15N]glutamine. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2362547&form=6&db=m Influence of acute metabolic acidosis on the monomer and polymer forms of renal phosphate-dependent glutaminase. ongoing research,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2563203&form=6&db=m Ammoniagenesis by cultured human renal cortical epithelial cells: study with 15N. causal interaction,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2665746&form=6&db=m Perturbations in nitrogen metabolism of brain and liver of rat following repeated benthiocarb administration. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2801694&form=6&db=m Response of ammonia metabolism to acute acidosis: insights from cultured renal epithelium. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2872677&form=6&db=m Hepatic enzymes of glutamine and ureagenesis in metabolic acidosis. causal interaction,diagnostic usage,unassigned 3,2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3191704&form=6&db=m Regulation of renal glutaminase gene expression during metabolic acidosis. ongoing research,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3300906&form=6&db=m Renal ammonium production--une vue canadienne. causal interaction,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3322041&form=6&db=m Interorgan glutamine flow in metabolic acidosis. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3569695&form=6&db=m The maximal activity of phosphate-dependent glutaminase and glutamine metabolism in the colon and the small intestine of streptozotocin-diabetic rats. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3606991&form=6&db=m Changes in the levels of translatable glutaminase mRNA during onset and recovery from metabolic acidosis. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3718673&form=6&db=m Hepatic glutaminase flux regulation of glutamine homeostasis. Studies in vivo. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3954723&form=6&db=m The effect of metabolic acidosis on the synthesis and turnover of rat renal phosphate-dependent glutaminase. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3963187&form=6&db=m Regulation of interorganal glutamine flow in metabolic acidosis. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4010646&form=6&db=m Relationship of phosphate-dependent glutaminase activity to ammonia excretion in potassium deficiency and acidosis. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5433558&form=6&db=m Effect of ischaemia and acidosis on glutaminase activity in the rat kidney. ongoing research,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6119101&form=6&db=m [Activity of renal enzymes producing ammonia from glutamine in the absence of phosphate in the rat: 1. Effect of chronic metabolic acidosis] diagnostic usage,ongoing research,unassigned 2,3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6122544&form=6&db=m Glutamine metabolism in metabolic acidosis. causal interaction,unassigned 2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6131695&form=6&db=m Regulation of flux through glutaminase and glutamine synthetase in isolated perfused rat liver. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6137960&form=6&db=m Renal ammoniagenesis and acid excretion in the dogfish, Squalus acanthias. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6231975&form=6&db=m Renal enzymes during experimental diabetes mellitus in the rat. Role of insulin, carbohydrate metabolism, and ketoacidosis. causal interaction,ongoing research,unassigned 3,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6508757&form=6&db=m The regulation of phosphate-activated glutaminase activity and glutamine metabolism in the streptozotocin-diabetic rat. diagnostic usage,therapeutic application,unassigned 1,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6813556&form=6&db=m The kidney of chicken adapts to chronic metabolic acidosis: in vivo and in vitro studies. therapeutic application,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7332866&form=6&db=m Renal metabolite concentrations and the activities of glutaminase and glutamate dehydrogenase during recovery from metabolic acidosis in the rat. ongoing research,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7409750&form=6&db=m The role of pH and the lack of a requirement for hydorgencarbonate in the regulation of hepatic glutamine metabolism. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7731175&form=6&db=m Hormonal regulation of glutamine metabolism by OK cells. therapeutic application,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8499480&form=6&db=m Phosphate-dependent glutaminase of rat skeletal muscle. Some properties and possible role in glutamine metabolism. ongoing research,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8527215&form=6&db=m Regulation of glutaminase activity and glutamine metabolism. causal interaction,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8638675&form=6&db=m Response of LLC-PK1-F+ cells to metabolic acidosis. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10966482&form=6&db=m Effect of acidosis on the properties of the glutaminase mRNA pH-response element binding protein. ongoing research,unassigned 2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12045296&form=6&db=m Complexity and species variation of the kidney-type glutaminase gene. causal interaction,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12684230&form=6&db=m pH-responsive stabilization of glutamate dehydrogenase mRNA in LLC-PK1-F+ cells. causal interaction,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12908170&form=6&db=m [Nephrogenic metabolic acidosis] diagnostic usage,unassigned 3,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15607573&form=6&db=m Acid-base balance may influence risk for insulin resistance syndrome by modulating cortisol output. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16219914&form=6&db=m Role of deadenylation and AUF1 binding in the pH-responsive stabilization of glutaminase mRNA. causal interaction,ongoing research,unassigned 4,2,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19657324&form=6&db=m Zeta-crystallin mediates the acid pH-induced increase of BSC1 cotransporter mRNA stability. causal interaction,unassigned 1,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24808535&form=6&db=m pH-responsive, gluconeogenic renal epithelial LLC-PK1-FBPase+cells: a versatile in vitro model to study renal proximal tubule metabolism and function. unassigned - 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25085245&form=6&db=m The SIRT1/HIF2? axis drives reductive glutamine metabolism under chronic acidosis and alters tumor response to therapy. therapeutic application,unassigned 4,0 3.5.1.2 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33966211&form=6&db=m Impact of Acidosis-Regulated MicroRNAs on the Expression of Their Target Genes in Experimental Tumors In Vivo. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Acidosis, Respiratory http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7409750&form=6&db=m The role of pH and the lack of a requirement for hydorgencarbonate in the regulation of hepatic glutamine metabolism. causal interaction,unassigned 3,0 3.5.1.2 Acute Kidney Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=919372&form=6&db=m [Activity of glutamine deaminating enzymes in the kidneys, liver and serum of dogs with renal failure and under normal conditions] unassigned - 3.5.1.2 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28611197&form=6&db=m Treatment of Pancreatic Cancer Patient-Derived Xenograft Panel with Metabolic Inhibitors Reveals Efficacy of Phenformin. therapeutic application,unassigned 4,0 3.5.1.2 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33947068&form=6&db=m Evaluation of Glutaminase Expression in Prostate Adenocarcinoma and Correlation with Clinicopathologic Parameters. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 3.5.1.2 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33991485&form=6&db=m SUCLA2-coupled regulation of GLS succinylation and activity counteracts oxidative stress in tumor cells. ongoing research,unassigned 1,0 3.5.1.2 Adenocarcinoma of Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30250881&form=6&db=m Dual targeting of EGFR and glutaminase in lung cancer. causal interaction,ongoing research,unassigned 4,2,0 3.5.1.2 Adenocarcinoma of Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040157&form=6&db=m LKB1 and KEAP1/NRF2 Pathways Cooperatively Promote Metabolic Reprogramming with Enhanced Glutamine Dependence in KRAS-Mutant Lung Adenocarcinoma. causal interaction,unassigned 2,0 3.5.1.2 Adenoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12408749&form=6&db=m Glutaminase isoform expression in cell lines derived from human colorectal adenomas and carcinomas. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 AIDS Dementia Complex http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22016553&form=6&db=m Glutaminase dysregulation in HIV-1-infected human microglia mediates neurotoxicity: relevant to HIV-1-associated neurocognitive disorders. causal interaction,diagnostic usage,unassigned 3,4,0 3.5.1.2 AIDS Dementia Complex http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24086752&form=6&db=m STAT1 Regulates Human Glutaminase 1 Promoter Activity through Multiple Binding Sites in HIV-1 Infected Macrophages. ongoing research,therapeutic application,unassigned 1,1,0 3.5.1.2 Alkalosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1600351&form=6&db=m Metabolic alkalosis as driving force for urea synthesis in liver disease: pathogenetic model and therapeutic implications. unassigned - 3.5.1.2 Alkalosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3569695&form=6&db=m The maximal activity of phosphate-dependent glutaminase and glutamine metabolism in the colon and the small intestine of streptozotocin-diabetic rats. unassigned - 3.5.1.2 Alkalosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6131695&form=6&db=m Regulation of flux through glutaminase and glutamine synthetase in isolated perfused rat liver. unassigned - 3.5.1.2 Alkalosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6508757&form=6&db=m The regulation of phosphate-activated glutaminase activity and glutamine metabolism in the streptozotocin-diabetic rat. diagnostic usage,therapeutic application,unassigned 1,1,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2213015&form=6&db=m Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,1,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2554171&form=6&db=m Excitatory amino acids and Alzheimer's disease: idle thoughts on an exciting subject. unassigned - 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2804813&form=6&db=m Cortical glutaminase, beta-glucuronidase and glucose utilization in Alzheimer's disease. causal interaction,diagnostic usage,unassigned 3,1,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2898011&form=6&db=m Topographical distribution of neurochemical changes in Alzheimer's disease. causal interaction,unassigned 2,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11523427&form=6&db=m [Impaired cerebral glutamate metabolism in mental diseases (Alzheimer's disease, schizophrenia] causal interaction,diagnostic usage,unassigned 3,3,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12091195&form=6&db=m Implications for altered glutamate and GABA metabolism in the dorsolateral prefrontal cortex of aged schizophrenic patients. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16341942&form=6&db=m Glutamate metabolizing enzymes in prefrontal cortex of Alzheimer's disease patients. diagnostic usage,unassigned 3,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24430039&form=6&db=m [Glutaminase in the cerebellum of patients with Alzheimer's disease: a postmortem brain study]. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24950944&form=6&db=m Glutamate and GABA-Metabolizing Enzymes in Post-mortem Cerebellum in Alzheimer's Disease: Phosphate-Activated Glutaminase and Glutamic Acid Decarboxylase. unassigned - 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26461365&form=6&db=m APC/Cdh E3 ubiquitin ligase in the pathophysiology of Alzheimer?s disease. causal interaction,unassigned 3,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28439409&form=6&db=m Serial deletion reveals structural basis and stability for the core enzyme activity of human glutaminase 1 isoforms: relevance to excitotoxic neurodegeneration. diagnostic usage,therapeutic application,unassigned 2,1,0 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31316350&form=6&db=m Glutaminase C Regulates Microglial Activation and Pro-inflammatory Exosome Release: Relevance to the Pathogenesis of Alzheimer's Disease. unassigned - 3.5.1.2 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32117296&form=6&db=m Glutaminase 1 Regulates Neuroinflammation After Cerebral Ischemia Through Enhancing Microglial Activation and Pro-Inflammatory Exosome Release. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Amyotrophic Lateral Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28439409&form=6&db=m Serial deletion reveals structural basis and stability for the core enzyme activity of human glutaminase 1 isoforms: relevance to excitotoxic neurodegeneration. diagnostic usage,therapeutic application,unassigned 2,1,0 3.5.1.2 Anemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4424429&form=6&db=m [Glutaminase activity in rabbit reticulocytes: determination and behavior during a blood-loss anemia] ongoing research,unassigned 2,0 3.5.1.2 Anemia, Hemolytic, Autoimmune http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31326291&form=6&db=m Anti tissue transglutaminase antibody in idiopathic autoimmune haemolytic anemia. ongoing research,unassigned 2,0 3.5.1.2 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28399896&form=6&db=m Glutaminase 1 plays a key role in the cell growth of fibroblast-like synoviocytes in rheumatoid arthritis. causal interaction,unassigned 3,0 3.5.1.2 Asthma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17110506&form=6&db=m Airway nitric oxide release is reduced after PBS inhalation in asthma. causal interaction,unassigned 4,0 3.5.1.2 Astrocytoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33910646&form=6&db=m Glutaminolysis dynamics during astrocytoma progression correlates with tumor aggressiveness. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,3,0 3.5.1.2 Ataxia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32121257&form=6&db=m Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats. unassigned - 3.5.1.2 Ataxia Telangiectasia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31449760&form=6&db=m Defining and targeting wild-type BRCA high-grade serous ovarian cancer: DNA repair and cell cycle checkpoints. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Brain Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25329718&form=6&db=m THDP17 decreases ammonia production through glutaminase inhibition. A new drug for hepatic encephalopathy therapy. therapeutic application,unassigned 4,0 3.5.1.2 Brain Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28439409&form=6&db=m Serial deletion reveals structural basis and stability for the core enzyme activity of human glutaminase 1 isoforms: relevance to excitotoxic neurodegeneration. diagnostic usage,therapeutic application,unassigned 2,1,0 3.5.1.2 Brain Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30239721&form=6&db=m GLS hyperactivity causes glutamate excess, infantile cataract and profound developmental delay. causal interaction,ongoing research,unassigned 1,1,0 3.5.1.2 Brain Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30575854&form=6&db=m Identification of a Loss-of-Function Mutation in the Context of Glutaminase Deficiency and Neonatal Epileptic Encephalopathy. causal interaction,unassigned 4,0 3.5.1.2 Brain Ischemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9824679&form=6&db=m Characterization of mitochondrial glutaminase and amino acids at prolonged times after experimental focal cerebral ischemia. ongoing research,therapeutic application,unassigned 2,3,0 3.5.1.2 Brain Ischemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32117296&form=6&db=m Glutaminase 1 Regulates Neuroinflammation After Cerebral Ischemia Through Enhancing Microglial Activation and Pro-Inflammatory Exosome Release. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Brain Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25837287&form=6&db=m Glutaminases in brain: Multiple isoforms for many purposes. causal interaction,unassigned 3,0 3.5.1.2 Brain Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33106333&form=6&db=m Brain Tumor Stem Cell Dependence on Glutaminase Reveals a Metabolic Vulnerability through the Amino Acid Deprivation Response Pathway. ongoing research,unassigned 1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10620514&form=6&db=m Molecular cloning, sequencing and expression studies of the human breast cancer cell glutaminase. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11015561&form=6&db=m Cloning and analysis of unique human glutaminase isoforms generated by tissue-specific alternative splicing. unassigned - 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12408749&form=6&db=m Glutaminase isoform expression in cell lines derived from human colorectal adenomas and carcinomas. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12758143&form=6&db=m Expression of recombinant human L-glutaminase in Escherichia coli: polyclonal antibodies production and immunological analysis of mouse tissues. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17614351&form=6&db=m Antisense glutaminase inhibition modifies the O-GlcNAc pattern and flux through the hexosamine pathway in breast cancer cells. causal interaction,ongoing research,therapeutic application,unassigned 1,4,1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18584486&form=6&db=m Glutamine affects glutathione recycling enzymes in a DMBA-induced breast cancer model. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20832749&form=6&db=m Targeting mitochondrial glutaminase activity inhibits oncogenic transformation. causal interaction,unassigned 3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23117580&form=6&db=m Modifying metabolically sensitive histone marks by inhibiting glutamine metabolism affects gene expression and alters cancer cell phenotype. causal interaction,ongoing research,therapeutic application,unassigned 1,3,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23507704&form=6&db=m Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer. diagnostic usage,ongoing research,unassigned 4,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24122876&form=6&db=m ErbB2 activation upregulates glutaminase 1 expression which promotes breast cancer cell proliferation. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24316975&form=6&db=m MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis. ongoing research,unassigned 1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24523301&form=6&db=m Antitumor Activity of the Glutaminase Inhibitor CB-839 in Triple-Negative Breast Cancer. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25683269&form=6&db=m Cross-talk between ER and HER2 regulates c-MYC-mediated glutamine metabolism in aromatase inhibitor resistant breast cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,3,4,1 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26988803&form=6&db=m Design and evaluation of novel glutaminase inhibitors. unassigned - 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27419628&form=6&db=m Glutamine deprivation plus BPTES alters etoposide- and cisplatin-induced apoptosis in triple negative breast cancer cells. ongoing research,therapeutic application,unassigned 3,1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30072394&form=6&db=m Glutamate-Weighted Chemical Exchange Saturation Transfer Magnetic Resonance Imaging Detects Glutaminase Inhibition in a Mouse Model of Triple-Negative Breast Cancer. therapeutic application,unassigned 3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30092248&form=6&db=m N-terminal phosphorylation of glutaminase C decreases its enzymatic activity and cancer cell migration. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040181&form=6&db=m Dual inhibition of glutaminase and carnitine palmitoyltransferase decreases growth and migration of glutaminase inhibition-resistant triple-negative breast cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,3,3 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31088535&form=6&db=m Glutamine to proline conversion is associated with response to glutaminase inhibition in breast cancer. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31189611&form=6&db=m Targeting Mitochondrial Proline Dehydrogenase with a Suicide Inhibitor to Exploit Synthetic Lethal Interactions with p53 Upregulation and Glutaminase Inhibition. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31577957&form=6&db=m Liver-Type Glutaminase GLS2 Is a Druggable Metabolic Node in Luminal-Subtype Breast Cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31596504&form=6&db=m The role of glutaminase in cancer. causal interaction,ongoing research,unassigned 3,3,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31843902&form=6&db=m SIRT5 stabilizes mitochondrial glutaminase and supports breast cancer tumorigenesis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,2 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32360595&form=6&db=m Vitamin D regulation of HAS2, hyaluronan synthesis and metabolism in triple negative breast cancer cells. unassigned - 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32450839&form=6&db=m Pyruvate anaplerosis is a mechanism of resistance to pharmacological glutaminase inhibition in triple-receptor negative breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,3,3,4 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32899149&form=6&db=m In Situ Metabolic Characterisation of Breast Cancer and Its Potential Impact on Therapy. diagnostic usage,ongoing research,unassigned 4,2,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33277391&form=6&db=m Kinetic Modeling of 18F-(2S,4R)4-Fluoroglutamine in Mouse Models of Breast Cancer to Estimate Glutamine Pool Size as an Indicator of Tumor Glutamine Metabolism. ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34354052&form=6&db=m Compound 968 reverses adriamycin resistance in breast cancer MCF-7ADR cells via inhibiting P-glycoprotein function independently of glutaminase. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34439127&form=6&db=m The Biological and Clinical Significance of Glutaminase in Luminal Breast Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24797434&form=6&db=m Glutaminase 2 negatively regulates the PI3K/AKT signaling and shows tumor suppression activity in human hepatocellular carcinoma. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25915584&form=6&db=m Targeted inhibition of tumor-specific glutaminase diminishes cell-autonomous tumorigenesis. causal interaction,therapeutic application,unassigned 2,2,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28168879&form=6&db=m Head and Neck Squamous Cell Carcinoma Metabolism Draws on Glutaminolysis, and Stemness Is Specifically Regulated by Glutaminolysis via Aldehyde Dehydrogenase. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28498807&form=6&db=m Knockdown of PKM2 and GLS1 expression can significantly reverse oxaliplatin-resistance in colorectal cancer cells. unassigned - 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29515166&form=6&db=m Phosphorylation of glutaminase by PKC? is essential for its enzymatic activity and critically contributes to tumorigenesis. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30669455&form=6&db=m Transfection with GLS2 Glutaminase (GAB) Sensitizes Human Glioblastoma Cell Lines to Oxidative Stress by a Common Mechanism Involving Suppression of the PI3K/AKT Pathway. ongoing research,unassigned 2,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31734463&form=6&db=m Metabolic fingerprinting reveals extensive consequences of GLS hyperactivity. unassigned - 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31843902&form=6&db=m SIRT5 stabilizes mitochondrial glutaminase and supports breast cancer tumorigenesis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,2 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32328963&form=6&db=m Molecular modeling and LC-MS-based metabolomics of a glutamine-valproic acid (Gln-VPA) derivative on HeLa cells. causal interaction,ongoing research,unassigned 3,1,0 3.5.1.2 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32694609&form=6&db=m Identifying strategies to target the metabolic flexibility of tumours. causal interaction,unassigned 1,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=363626&form=6&db=m Mechanism of sensitivity of cultured pancreatic carcinoma to asparaginase. causal interaction,diagnostic usage,ongoing research,unassigned 3,2,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=990468&form=6&db=m [Concentration of free glutamine and glutaminase activity in the gastric mucosa of patients with precancerous diseases and cancer of the stomach] diagnostic usage,ongoing research,unassigned 1,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1346587&form=6&db=m Glutaminase and glutamine synthetase activities in human cirrhotic liver and hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3342022&form=6&db=m Amino acid metabolism in tumour-bearing mice. causal interaction,unassigned 1,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4930322&form=6&db=m Glutaminase induced prolonged regression of established Ehrlich carcinoma. unassigned - 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5761007&form=6&db=m [Action of swine kidney L-glutaminase on Ehrlich carcinoma] diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8137919&form=6&db=m Phosphate-activated glutaminase expression during tumor development. causal interaction,ongoing research,unassigned 4,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9929166&form=6&db=m Early differential expression of two glutaminase mRNAs in mouse spleen after tumor implantation. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11033463&form=6&db=m Localization of phosphate dependent glutaminase in ascites fluid of ovarian cancer patient. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,1,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12408749&form=6&db=m Glutaminase isoform expression in cell lines derived from human colorectal adenomas and carcinomas. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21854356&form=6&db=m Expanding Targets for a Metabolic Therapy of Cancer: L-Asparaginase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27829138&form=6&db=m Targeting Stromal Glutamine Synthetase in Tumors Disrupts Tumor Microenvironment-Regulated Cancer Cell Growth. ongoing research,unassigned 2,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28462847&form=6&db=m Breaking the ritual metabolic cycle in order to save acetyl CoA: A potential role for mitochondrial humanin in T2 bladder cancer aggressiveness. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29763620&form=6&db=m Targeting Therapy Resistance: When Glutamine Catabolism Becomes Essential. causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30854496&form=6&db=m The 'Achilles Heel' of Metabolism in Renal Cell Carcinoma: Glutaminase Inhibition as a Rational Treatment Strategy. therapeutic application,unassigned 4,0 3.5.1.2 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33450358&form=6&db=m Glutaminase inhibition with telaglenastat (CB-839) improves treatment response in combination with ionizing radiation in head and neck squamous cell carcinoma models. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Carcinoma, Ductal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34439127&form=6&db=m The Biological and Clinical Significance of Glutaminase in Luminal Breast Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4429959&form=6&db=m Properties and intracellular localization of Ehrlich ascites tumor cell glutaminase. ongoing research,unassigned 4,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10816417&form=6&db=m Inhibition of glutaminase expression by antisense mRNA decreases growth and tumourigenicity of tumour cells. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10928057&form=6&db=m Changes in mRNAs for enzymes of glutamine metabolism in the tumor-bearing mouse. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11169963&form=6&db=m Ehrlich ascites tumor cells expressing anti-sense glutaminase mRNA lose their capacity to evade the mouse immune system. causal interaction,ongoing research,therapeutic application,unassigned 4,3,2,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15511236&form=6&db=m Antisense glutaminase inhibition decreases glutathione antioxidant capacity and increases apoptosis in Ehrlich ascitic tumour cells. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16101144&form=6&db=m Sensitisation of Ehrlich ascitic tumour cells to methotrexate by inhibiting glutaminase. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Carcinoma, Ehrlich Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16294018&form=6&db=m Identification of genes downregulated in tumor cells expressing antisense glutaminase mRNA by differential display. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Carcinoma, Embryonal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27322683&form=6&db=m Autocrine glutamatergic transmission for the regulation of embryonal carcinoma stem cells. ongoing research,unassigned 4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=195624&form=6&db=m Glutaminase activity of glutamine-dependent carbamoyl-phosphate synthase from rat ascites hepatoma. Regulation by adenosine triphosphate-magensium and magnesium ion. ongoing research,unassigned 1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1346587&form=6&db=m Glutaminase and glutamine synthetase activities in human cirrhotic liver and hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1991024&form=6&db=m Biosynthesis and processing of mitochondrial glutaminase in HTC hepatoma cells. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2573354&form=6&db=m Glutamine synthetase and glutaminase activities in various hepatoma cells. causal interaction,diagnostic usage,ongoing research,unassigned 1,2,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4307782&form=6&db=m Glutaminase activities and growth rates of rat hepatomas. ongoing research,unassigned 3,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4320028&form=6&db=m Anomalous distribution of glutaminase isozyme in various hepatomas. ongoing research,unassigned 2,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7944654&form=6&db=m Modulation of cellular proliferation alters glutamine transport and metabolism in human hepatoma cells. diagnostic usage,ongoing research,unassigned 1,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9164856&form=6&db=m Rat hepatic glutaminase: identification of the full coding sequence and characterization of a functional promoter. ongoing research,unassigned 2,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18666104&form=6&db=m 1C MR spectroscopy measurements of glutaminase activity in human hepatocellular carcinoma cells using hyperpolarized 13C-labeled glutamine. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23873638&form=6&db=m Biochemical Characterization and Antitumor Study of L-Glutaminase from Bacillus cereus MTCC 1305. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24797434&form=6&db=m Glutaminase 2 negatively regulates the PI3K/AKT signaling and shows tumor suppression activity in human hepatocellular carcinoma. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25844758&form=6&db=m Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 2,4,1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27725225&form=6&db=m Glutaminase 2 stabilizes Dicer to repress Snail and metastasis in hepatocellular carcinoma cells. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,3,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27835669&form=6&db=m The Glutaminase-1 Inhibitor 968 Enhances Dihydroartemisinin-Mediated Antitumor Efficacy in Hepatocellular Carcinoma Cells. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29988727&form=6&db=m Nuclear factor-?B p65 regulates glutaminase 1 expression in human hepatocellular carcinoma. ongoing research,unassigned 2,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30555042&form=6&db=m Targeting glutaminase 1 attenuates stemness properties in hepatocellular carcinoma by increasing reactive oxygen species and suppressing Wnt/beta-catenin pathway. ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30786811&form=6&db=m The HGF-MET axis coordinates liver cancer metabolism and autophagy for chemotherapeutic resistance. diagnostic usage,therapeutic application,unassigned 1,1,0 3.5.1.2 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31743703&form=6&db=m Purification and characterization of l-glutaminase enzyme from camel liver: Enzymatic anticancer property. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,4 3.5.1.2 Carcinoma, Intraductal, Noninfiltrating http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34439127&form=6&db=m The Biological and Clinical Significance of Glutaminase in Luminal Breast Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.5.1.2 Carcinoma, Lewis Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3342022&form=6&db=m Amino acid metabolism in tumour-bearing mice. causal interaction,unassigned 1,0 3.5.1.2 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26575584&form=6&db=m Inhibition of mitochondrial glutaminase activity reverses acquired erlotinib resistance in non-small cell lung cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27929535&form=6&db=m Dual targeting of glutaminase 1 and thymidylate synthase elicits death synergistically in NSCLC. causal interaction,unassigned 4,0 3.5.1.2 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28039459&form=6&db=m A novel glutaminase inhibitor-968 inhibits the migration and proliferation of non-small cell lung cancer cells by targeting EGFR/ERK signaling pathway. ongoing research,unassigned 2,0 3.5.1.2 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040157&form=6&db=m LKB1 and KEAP1/NRF2 Pathways Cooperatively Promote Metabolic Reprogramming with Enhanced Glutamine Dependence in KRAS-Mutant Lung Adenocarcinoma. causal interaction,unassigned 2,0 3.5.1.2 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30854496&form=6&db=m The 'Achilles Heel' of Metabolism in Renal Cell Carcinoma: Glutaminase Inhibition as a Rational Treatment Strategy. therapeutic application,unassigned 4,0 3.5.1.2 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29763620&form=6&db=m Targeting Therapy Resistance: When Glutamine Catabolism Becomes Essential. causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33450358&form=6&db=m Glutaminase inhibition with telaglenastat (CB-839) improves treatment response in combination with ionizing radiation in head and neck squamous cell carcinoma models. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Carcinosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15850218&form=6&db=m [The regulatory action of dipeptide "Deglutam" on the glutamine metabolized enzymes in the carcinosarcoma SM-1 cells] ongoing research,unassigned 2,0 3.5.1.2 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34014548&form=6&db=m Metabolic Intersection of Cancer and Cardiovascular Diseases: Opportunities for Cancer Therapy. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Cataract http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30239721&form=6&db=m GLS hyperactivity causes glutamate excess, infantile cataract and profound developmental delay. causal interaction,ongoing research,unassigned 1,1,0 3.5.1.2 Celiac Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5660603&form=6&db=m Small intestine glutaminase deficiency in celiac disease. causal interaction,diagnostic usage,unassigned 3,3,0 3.5.1.2 Central Nervous System Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23850693&form=6&db=m Kinetic characterization of ebselen, chelerythrine and apomorphine as glutaminase inhibitors. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Cholera http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11731099&form=6&db=m Evidence for glutamate, in addition to acetylcholine and GABA, neurotransmitter synthesis in basal forebrain neurons projecting to the entorhinal cortex. diagnostic usage,therapeutic application,unassigned 4,1,0 3.5.1.2 Chondrosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29576625&form=6&db=m Targeting glutaminolysis in chondrosarcoma in context of the IDH1/2 mutation. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24330717&form=6&db=m Epigenetic silencing of glutaminase 2 in human liver and colon cancers. ongoing research,unassigned 4,0 3.5.1.2 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31303578&form=6&db=m Inhibition of Glucose Transporters and Glutaminase Synergistically Impairs Tumor Cell Growth. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.5.1.2 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31788130&form=6&db=m A combination of inhibitors of glycolysis, glutaminolysis and de novo fatty acid synthesis decrease the expression of chemokines in human colon cancer cells. diagnostic usage,ongoing research,unassigned 2,3,0 3.5.1.2 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33004309&form=6&db=m A facile and sensitive method of quantifying glutaminase binding to its inhibitor CB-839 in tissues. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,3 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24696726&form=6&db=m Expression of glutaminase is upregulated in colorectal cancer and of clinical significance. causal interaction,diagnostic usage,unassigned 4,3,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28928849&form=6&db=m Glutaminase sustains cell survival via the regulation of glycolysis and glutaminolysis in colorectal cancer. diagnostic usage,unassigned 1,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30674873&form=6&db=m Glutaminase 1 expression in colorectal cancer cells is induced by hypoxia and required for tumor growth, invasion, and metastatic colonization. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32218849&form=6&db=m Intratumoral heterogeneity of glutaminase and lactate dehydrogenase A protein expression in colorectal cancer. causal interaction,diagnostic usage,unassigned 1,3,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32907836&form=6&db=m 5-fluorouracil enhances the anti-tumor activity of the glutaminase inhibitor CB-839 against PIK3CA-mutant colorectal cancers. causal interaction,diagnostic usage,therapeutic application,unassigned 2,3,2,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33807313&form=6&db=m L-Glutaminase Synthesis by Marine Halomonas meridiana Isolated from the Red Sea and Its Efficiency against Colorectal Cancer Cell Lines. ongoing research,therapeutic application,unassigned 2,4,0 3.5.1.2 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34119480&form=6&db=m GLS1 depletion inhibited colorectal cancer proliferation and migration via redox/Nrf2/autophagy-dependent pathway. causal interaction,unassigned 3,0 3.5.1.2 Coma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20487986&form=6&db=m Acute metabolic effects of ammonia on the enzymes of glutamate metabolism in isolated astroglial cells. unassigned - 3.5.1.2 Crohn Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17078002&form=6&db=m Low intestinal glutamine level and low glutaminase activity in Crohn's disease: a rational for glutamine supplementation? diagnostic usage,ongoing research,unassigned 3,2,0 3.5.1.2 Crush Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=13305835&form=6&db=m [Enzymatic activity in the organism in experimental crush syndrome of the limbs. III. Arginase in kidney and liver, glutaminase in kidney.] unassigned - 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2165009&form=6&db=m Is the neuronal basis of Alzheimer's disease cholinergic or glutamatergic? causal interaction,diagnostic usage,therapeutic application,unassigned 1,2,1,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2213015&form=6&db=m Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,1,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14675161&form=6&db=m Mitochondrial glutaminase enhances extracellular glutamate production in HIV-1-infected macrophages: linkage to HIV-1 associated dementia. causal interaction,unassigned 2,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18059978&form=6&db=m Potentiation of Excitotoxicity in HIV-1 Associated Dementia and the Significance of Glutaminase. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,1,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18088378&form=6&db=m HIV-infected macrophages mediate neuronal apoptosis through mitochondrial glutaminase. causal interaction,therapeutic application,unassigned 1,4,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23850693&form=6&db=m Kinetic characterization of ebselen, chelerythrine and apomorphine as glutaminase inhibitors. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Dementia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24269238&form=6&db=m Small molecule glutaminase inhibitors block glutamate release from stimulated microglia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Diabetes Mellitus http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23180316&form=6&db=m Role of diabetes mellitus on hepatic encephalopathy. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Diabetes Mellitus, Experimental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4157228&form=6&db=m [Glutamine synthetase and glutaminase activity in the brain and liver homogenates and subcellular fractions of rats with alloxan diabetes (3)] ongoing research,unassigned 3,0 3.5.1.2 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23180316&form=6&db=m Role of diabetes mellitus on hepatic encephalopathy. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Diabetic Ketoacidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3089169&form=6&db=m Effect of diabetic ketosis on jejunal glutaminase. ongoing research,unassigned 3,0 3.5.1.2 Down Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2213015&form=6&db=m Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,1,0 3.5.1.2 Encephalitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23578284&form=6&db=m IL-1? and TNF-? induce neurotoxicity through glutamate production: a potential role for neuronal glutaminase. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Encephalomyelitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19212100&form=6&db=m Blockade of glutamate release from microglia attenuates experimental autoimmune encephalomyelitis in mice. ongoing research,unassigned 4,0 3.5.1.2 Encephalomyelitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31233276&form=6&db=m Glutaminase 1 Inhibition Reduces Glycolysis and Ameliorates Lupus-like Disease in MRL/lpr Mice and Experimental Autoimmune Encephalomyelitis. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Encephalomyelitis, Autoimmune, Experimental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19212100&form=6&db=m Blockade of glutamate release from microglia attenuates experimental autoimmune encephalomyelitis in mice. ongoing research,unassigned 4,0 3.5.1.2 Encephalomyelitis, Autoimmune, Experimental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31233276&form=6&db=m Glutaminase 1 Inhibition Reduces Glycolysis and Ameliorates Lupus-like Disease in MRL/lpr Mice and Experimental Autoimmune Encephalomyelitis. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Endometrial Hyperplasia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32401642&form=6&db=m Autophagy in the physiological endometrium and cancer. unassigned - 3.5.1.2 Endometrial Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32401642&form=6&db=m Autophagy in the physiological endometrium and cancer. unassigned - 3.5.1.2 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1350313&form=6&db=m Adaptive regulation in skeletal muscle glutamine metabolism in endotoxin-treated rats. diagnostic usage,unassigned 1,0 3.5.1.2 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7637340&form=6&db=m Activation of hepatic glutaminase in the endotoxin-treated rat. causal interaction,unassigned 3,0 3.5.1.2 Eosinophilia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33558372&form=6&db=m Targeting In Vivo Metabolic Vulnerabilities of Th2 and Th17 Cells Reduces Airway Inflammation. therapeutic application,unassigned 3,0 3.5.1.2 Epilepsy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17115168&form=6&db=m Increased expression of phosphate-activated glutaminase in hippocampal neurons in human mesial temporal lobe epilepsy. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Epilepsy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25345404&form=6&db=m The anticonvulsant actions of carisbamate associate with alterations in astrocyte glutamine metabolism in the lithium-pilocarpine epilepsy model. unassigned - 3.5.1.2 Epilepsy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27885637&form=6&db=m The Glutamate-Glutamine Cycle in Epilepsy. causal interaction,unassigned 1,0 3.5.1.2 Epilepsy, Temporal Lobe http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17115168&form=6&db=m Increased expression of phosphate-activated glutaminase in hippocampal neurons in human mesial temporal lobe epilepsy. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Fatty Liver http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32084378&form=6&db=m Targeting Hepatic Glutaminase 1 Ameliorates Non-alcoholic Steatohepatitis by Restoring Very-Low-Density Lipoprotein Triglyceride Assembly. unassigned - 3.5.1.2 Fibrosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9605654&form=6&db=m Adaptive alterations in cellular metabolism with malignant transformation. unassigned - 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21045145&form=6&db=m Inhibition of Glutaminase Preferentially Slows Growth of Glioma Cells with Mutant IDH1. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21555572&form=6&db=m Pyruvate carboxylase is required for glutamine-independent growth of tumor cells. causal interaction,ongoing research,unassigned 3,1,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22888977&form=6&db=m Transfection of a human glioblastoma cell line with liver-type glutaminase (LGA) down-regulates the expression of DNA repair gene MGMT and sensitizes the cells to alkylating agents. ongoing research,unassigned 4,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25529918&form=6&db=m Opposing roles of glutaminase isoforms in determining glioblastoma cell phenotype. diagnostic usage,unassigned 3,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26422827&form=6&db=m Alterations in cellular metabolome after pharmacological inhibition of Notch in glioblastoma cells. diagnostic usage,ongoing research,therapeutic application,unassigned 1,2,4,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28218035&form=6&db=m MicroRNA-153 regulates glutamine metabolism in glioblastoma through targeting glutaminase. therapeutic application,unassigned 2,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28939850&form=6&db=m Glutaminase 2 expression is associated with regional heterogeneity of 5-aminolevulinic acid fluorescence in glioblastoma. unassigned - 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30669455&form=6&db=m Transfection with GLS2 Glutaminase (GAB) Sensitizes Human Glioblastoma Cell Lines to Oxidative Stress by a Common Mechanism Involving Suppression of the PI3K/AKT Pathway. ongoing research,unassigned 2,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32337072&form=6&db=m A comparative pharmaco-metabolomic study of glutaminase inhibitors in glioma stem-like cells confirms biological effectiveness but reveals differences in target-specificity. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32726986&form=6&db=m Erratum: Majewska, E. et al. Transfection with GLS2 Glutaminase (GAB) Sensitizes Human Glioblastoma Cell Lines to Oxidative Stress by a Common Mechanism Involving Suppression of the PI3K/AKT Pathway. Cancers 2019, 11, 115. ongoing research,unassigned 2,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33179520&form=6&db=m Upregulation of glutaminase 2 and neutrophil cytosolic factor 2 is associated with the poor prognosis of glioblastoma. causal interaction,diagnostic usage,unassigned 4,2,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33529962&form=6&db=m Cassane diterpenoid derivative induces apoptosis in IDH1 mutant glioma cells through the inhibition of glutaminase in vitro and in vivo. ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33610185&form=6&db=m Glutaminase isoforms expression switches microRNA levels and oxidative status in glioblastoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,1 3.5.1.2 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33672398&form=6&db=m Augmented Therapeutic Potential of Glutaminase Inhibitor CB839 in Glioblastoma Stem Cells Using Gold Nanoparticle Delivery. ongoing research,therapeutic application,unassigned 1,4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15663956&form=6&db=m Lack of expression of the liver-type glutaminase (LGA) mRNA in human malignant gliomas. ongoing research,unassigned 4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19062176&form=6&db=m Transfection with liver-type glutaminase cDNA alters gene expression and reduces survival, migration and proliferation of T98G glioma cells. diagnostic usage,ongoing research,unassigned 2,3,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21045145&form=6&db=m Inhibition of Glutaminase Preferentially Slows Growth of Glioma Cells with Mutant IDH1. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22888977&form=6&db=m Transfection of a human glioblastoma cell line with liver-type glutaminase (LGA) down-regulates the expression of DNA repair gene MGMT and sensitizes the cells to alkylating agents. ongoing research,unassigned 4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24276018&form=6&db=m Both GLS silencing and GLS2 overexpression synergize with oxidative stress against proliferation of glioma cells. ongoing research,unassigned 3,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24944014&form=6&db=m Glutamate/glutamine metabolism coupling between astrocytes and glioma cells: neuroprotection and inhibition of glioma growth. unassigned - 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26922345&form=6&db=m Clinical aggressiveness of malignant gliomas is linked to augmented metabolism of amino acids. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30220459&form=6&db=m Transaminase Inhibition by 2-Hydroxyglutarate Impairs Glutamate Biosynthesis and Redox Homeostasis in Glioma. ongoing research,therapeutic application,unassigned 2,4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31187466&form=6&db=m Inhibition of Metabolic Shift can Decrease Therapy Resistance in Human High-Grade Glioma Cells. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32337072&form=6&db=m A comparative pharmaco-metabolomic study of glutaminase inhibitors in glioma stem-like cells confirms biological effectiveness but reveals differences in target-specificity. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33101674&form=6&db=m Metabolic plasticity of IDH1-mutant glioma cell lines is responsible for low sensitivity to glutaminase inhibition. therapeutic application,unassigned 4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33529962&form=6&db=m Cassane diterpenoid derivative induces apoptosis in IDH1 mutant glioma cells through the inhibition of glutaminase in vitro and in vivo. ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33681764&form=6&db=m The glutamine antagonist prodrug JHU-083 slows malignant glioma growth and disrupts mTOR signaling. causal interaction,ongoing research,unassigned 4,4,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34172075&form=6&db=m Impaired anaplerosis is a major contributor to glycolysis inhibitor toxicity in glioma. causal interaction,ongoing research,therapeutic application,unassigned 1,3,3,0 3.5.1.2 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34490096&form=6&db=m SNAP25 Inhibits Glioma Progression by Regulating Synapse Plasticity via GLS-Mediated Glutaminolysis. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,2,1 3.5.1.2 Gliosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25539862&form=6&db=m Cell-density-dependent manifestation of partial characteristics for neuronal precursors in a newly established human gliosarcoma cell line. ongoing research,unassigned 1,0 3.5.1.2 glutamate dehydrogenase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7424621&form=6&db=m The natural history of hyperuricemia among asymptomatic relatives of patients with gout. causal interaction,unassigned 3,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5660603&form=6&db=m Small intestine glutaminase deficiency in celiac disease. causal interaction,diagnostic usage,unassigned 3,3,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26778975&form=6&db=m Genetic Pharmacotherapy as an Early CNS Drug Development Strategy: Testing Glutaminase Inhibition for Schizophrenia Treatment in Adult Mice. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30552621&form=6&db=m Molecular Imaging of mGluR5 Availability with [11C]ABP68 in Glutaminase Heterozygous Mice. causal interaction,unassigned 4,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30575854&form=6&db=m Identification of a Loss-of-Function Mutation in the Context of Glutaminase Deficiency and Neonatal Epileptic Encephalopathy. causal interaction,unassigned 4,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30970188&form=6&db=m Glutaminase Deficiency Caused by Short Tandem Repeat Expansion in GLS. causal interaction,unassigned 3,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31532978&form=6&db=m Glutaminase Deficiency Caused by Short Tandem Repeat Expansion in GLS. causal interaction,unassigned 3,0 3.5.1.2 glutaminase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31532979&form=6&db=m Glutaminase Deficiency Caused by Short Tandem Repeat Expansion in GLS. Reply. causal interaction,unassigned 3,0 3.5.1.2 Gout http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5843084&form=6&db=m Glutaminase activity in the kidney in gout. ongoing research,unassigned 4,0 3.5.1.2 Graves Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8640958&form=6&db=m Metabolism of glucose and glutamine in lymphocytes from Graves' hyperthyroid patients: influence of methimazole treatment. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Head and Neck Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28168879&form=6&db=m Head and Neck Squamous Cell Carcinoma Metabolism Draws on Glutaminolysis, and Stemness Is Specifically Regulated by Glutaminolysis via Aldehyde Dehydrogenase. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.5.1.2 Hematologic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31387889&form=6&db=m Assessing Metabolic Intervention with a Glutaminase Inhibitor in Real-time by Hyperpolarized Magnetic Resonance in Acute Myeloid Leukemia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=440565&form=6&db=m [Activity of l-glutamine amidohydrolase in the rat brain in experimental hepatic encephalopathy] diagnostic usage,ongoing research,unassigned 2,4,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6119654&form=6&db=m [Ammonia content and glutamine synthetase and glutaminase activity in the brain in experimental hepatic coma] ongoing research,unassigned 1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8768304&form=6&db=m Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models. ongoing research,unassigned 1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15246207&form=6&db=m Intestinal glutaminase activity is increased in liver cirrhosis and correlates with minimal hepatic encephalopathy. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16382342&form=6&db=m Role of phosphate-activated glutaminase in the pathogenesis of hepatic encephalopathy. causal interaction,ongoing research,therapeutic application,unassigned 3,1,4,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16688834&form=6&db=m Phosphate-activated glutaminase activity is enhanced in brain, intestine and kidneys of rats following portacaval anastomosis. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19067141&form=6&db=m Gut ammonia production and its modulation. therapeutic application,unassigned 1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20820037&form=6&db=m Variations in the promoter region of the glutaminase gene and the development of hepatic encephalopathy in patients with cirrhosis: a cohort study. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,4,4,1 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23166628&form=6&db=m Metformin inhibits glutaminase activity and protects against hepatic encephalopathy. therapeutic application,unassigned 2,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23180316&form=6&db=m Role of diabetes mellitus on hepatic encephalopathy. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25329718&form=6&db=m THDP17 decreases ammonia production through glutaminase inhibition. A new drug for hepatic encephalopathy therapy. therapeutic application,unassigned 4,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25880019&form=6&db=m A genetic variant in the promoter of phosphate-activated glutaminase is associated with hepatic encephalopathy. unassigned - 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27749985&form=6&db=m Validation study associating glutaminase promoter variations with hepatic encephalopathy in East Asian populations. diagnostic usage,ongoing research,therapeutic application,unassigned 4,4,1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28439409&form=6&db=m Serial deletion reveals structural basis and stability for the core enzyme activity of human glutaminase 1 isoforms: relevance to excitotoxic neurodegeneration. diagnostic usage,therapeutic application,unassigned 2,1,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30646605&form=6&db=m Metformin Impairs Glutamine Metabolism and Autophagy in Tumour Cells. causal interaction,therapeutic application,unassigned 1,2,0 3.5.1.2 Hepatic Encephalopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31014748&form=6&db=m Pathophysiology of hepatic encephalopathy and future treatment options. unassigned - 3.5.1.2 Hepatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18647344&form=6&db=m Structural and functional insights into Erwinia carotovora L-asparaginase. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Hepatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24761390&form=6&db=m Cloning, expression, purification and characterisation of Erwinia carotovora L-asparaginase in Escherichia coli. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Herpes Simplex http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26561297&form=6&db=m MYC-induced reprogramming of glutamine catabolism supports optimal virus replication. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,1,0 3.5.1.2 Huntington Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2213015&form=6&db=m Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,1,0 3.5.1.2 Huntington Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2858515&form=6&db=m Distribution of phosphate-activated glutaminase, succinic dehydrogenase, pyruvate dehydrogenase and gamma-glutamyl transpeptidase in post-mortem brain from Huntington's disease and agonal cases. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,2,0 3.5.1.2 Huntington Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6223989&form=6&db=m Phosphate-activated glutaminase in relation to Huntington's disease and agonal state. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,1,3 3.5.1.2 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29578539&form=6&db=m Targeting hepatic glutaminase activity to ameliorate hyperglycemia. ongoing research,unassigned 1,0 3.5.1.2 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29895835&form=6&db=m Publisher Correction: Targeting hepatic glutaminase activity to ameliorate hyperglycemia. therapeutic application,unassigned 1,0 3.5.1.2 Hyperhomocysteinemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26935476&form=6&db=m Maternal vitamin B6 deficient or supplemented diets on expression of genes related to GABAergic, serotonergic or glutamatergic pathways in hippocampus of rat dams and their offspring. unassigned - 3.5.1.2 Hypersensitivity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33932739&form=6&db=m Circumventing the side effects of L-asparaginase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Hypertension, Pulmonary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34056915&form=6&db=m Simultaneous Pharmacologic Inhibition of Yes-Associated Protein 1 and Glutaminase 1 via Inhaled Poly(Lactic-co-Glycolic) Acid-Encapsulated Microparticles Improves Pulmonary Hypertension. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Hyperthyroidism http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7758149&form=6&db=m Effect of hypo- and hyperthyroidism on the function and metabolism of macrophages in rats. unassigned - 3.5.1.2 Hyperthyroidism http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8467960&form=6&db=m Effects of hyperthyroidism on glucose, glutamine and ketone-body metabolism in the gut of the rat. unassigned - 3.5.1.2 Hypoglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18663970&form=6&db=m [Parameters of energy and nitrogen metabolism in rats under insulin-induced hypoglycemia] unassigned - 3.5.1.2 Ichthyosis, Lamellar http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10733670&form=6&db=m Efficient in vitro transfection of human keratinocytes with an adenovirus-enhanced receptor-mediated system. ongoing research,unassigned 2,0 3.5.1.2 Ileitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17078002&form=6&db=m Low intestinal glutamine level and low glutaminase activity in Crohn's disease: a rational for glutamine supplementation? diagnostic usage,ongoing research,unassigned 3,2,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1361009&form=6&db=m Cerebral ammonia levels and enzyme changes during Plasmodium yoelii infection in mice. causal interaction,diagnostic usage,unassigned 2,2,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8343065&form=6&db=m Endotoxin stimulates lymphocyte glutaminase expression. causal interaction,unassigned 3,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10374488&form=6&db=m [Influence of recombinant growth hormone on protein metabolism during severe infection: an animal experiment] diagnostic usage,ongoing research,unassigned 3,1,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17596215&form=6&db=m Glutamate production by HIV-1 infected human macrophage is blocked by the inhibition of glutaminase. causal interaction,therapeutic application,unassigned 1,1,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19222703&form=6&db=m In vitro glutaminase regulation and mechanisms of glutamate generation in HIV-1-infected macrophage. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,1,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22479354&form=6&db=m Interferon-? regulates glutaminase 1 promoter through STAT1 phosphorylation: relevance to HIV-1 associated neurocognitive disorders. therapeutic application,unassigned 4,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22527635&form=6&db=m Mitochondrial Glutaminase Release Contributes to Glutamate-Mediated Neurotoxicity during Human Immunodeficiency Virus-1 Infection. ongoing research,therapeutic application,unassigned 4,1,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25299066&form=6&db=m Glutamate secretion and metabotropic glutamate receptor 1 expression during Kaposi's sarcoma-associated herpesvirus infection promotes cell proliferation. ongoing research,unassigned 3,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26546362&form=6&db=m Glutaminase-containing microvesicles from HIV-1-infected macrophages and immune-activated microglia induce neurotoxicity. causal interaction,unassigned 3,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27095107&form=6&db=m Proteomics and functional analyses of Arabidopsis nitrilases involved in the defense response to microbial pathogens. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27600401&form=6&db=m Glutamine was required for snakehead fish vesiculovirus (SHVV) propagation via replenishing the tricarboxylic acid cycle. unassigned - 3.5.1.2 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32214337&form=6&db=m Glutamine supplementation improves the efficacy of miltefosine treatment for visceral leishmaniasis. ongoing research,unassigned 3,0 3.5.1.2 Influenza, Human http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26561297&form=6&db=m MYC-induced reprogramming of glutamine catabolism supports optimal virus replication. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,1,0 3.5.1.2 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26446022&form=6&db=m Clinical science workshop: targeting the gut-liver-brain axis. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Ketosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6231975&form=6&db=m Renal enzymes during experimental diabetes mellitus in the rat. Role of insulin, carbohydrate metabolism, and ketoacidosis. causal interaction,ongoing research,unassigned 3,1,0 3.5.1.2 Kidney Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28346230&form=6&db=m Glutaminase and poly(ADP-ribose) polymerase inhibitors suppress pyrimidine synthesis and VHL-deficient renal cancers. causal interaction,therapeutic application,unassigned 2,3,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4526274&form=6&db=m L-glutaminase activity in lymphocytes of patients with chronic lymphatic leukemia. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,1,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7055814&form=6&db=m Tumoricidal potential of nutritional manipulations. therapeutic application,unassigned 4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18647344&form=6&db=m Structural and functional insights into Erwinia carotovora L-asparaginase. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18988465&form=6&db=m [Cloning, expression and purification of Helicobater pylori L-asparaginase] causal interaction,diagnostic usage,therapeutic application,unassigned 3,1,4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24362429&form=6&db=m Biochemical characterization of a novel L-Asparaginase with low glutaminase activity from Rhizomucor miehei and its application in food safety and leukemia treatment. therapeutic application,unassigned 4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24761390&form=6&db=m Cloning, expression, purification and characterisation of Erwinia carotovora L-asparaginase in Escherichia coli. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24905227&form=6&db=m Purification and characterization of a novel and robust L-asparaginase having low-glutaminase activity from Bacillus licheniformis: in vitro evaluation of anti-cancerous properties. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25941002&form=6&db=m Glutaminase activity determines cytotoxicity of L-asparaginases on most leukemia cell lines. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,2,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26597158&form=6&db=m Purification and characterization of glutaminase free asparaginase from Pseudomonas otitidis: Induce apoptosis in human leukemia MOLT-4 cells. causal interaction,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27806325&form=6&db=m Inhibiting glutaminase in acute myeloid leukemia: metabolic dependency of selected AML subtypes. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29343523&form=6&db=m A Novel l-Asparaginase with low l-Glutaminase Coactivity Is Highly Efficacious against Both T- and B-cell Acute Lymphoblastic Leukemias causal interaction,therapeutic application,unassigned 4,2,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31130824&form=6&db=m Effect of cold atmospheric plasma treatment on the metabolites of human leukemia cells. causal interaction,diagnostic usage,unassigned 1,3,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31209181&form=6&db=m Glutaminase Activity of L-Asparaginase Contributes to Durable Preclinical Activity against Acute Lymphoblastic Leukemia. diagnostic usage,ongoing research,therapeutic application,unassigned 1,3,2,0 3.5.1.2 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31297305&form=6&db=m l-Asparaginase from Aspergillus spp.: production based on kinetics, thermal stability and biochemical characterization. causal interaction,unassigned 1,0 3.5.1.2 Leukemia, Erythroblastic, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6572560&form=6&db=m Prominent glutamine oxidation activity in mitochondria of hematopoietic tumors. diagnostic usage,unassigned 1,0 3.5.1.2 Leukemia, Lymphocytic, Chronic, B-Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4526274&form=6&db=m L-glutaminase activity in lymphocytes of patients with chronic lymphatic leukemia. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,1,0 3.5.1.2 Leukemia, Myeloid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26891220&form=6&db=m Purification and Characterization of Glutaminase Free Asparaginase from Enterobacter cloacae: In-Vitro Evaluation of Cytotoxic Potential against Human Myeloid Leukemia HL-60 Cells. diagnostic usage,ongoing research,therapeutic application,unassigned 1,4,1,0 3.5.1.2 Leukemia, Myeloid, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24333121&form=6&db=m Inhibition of glutaminase selectively suppresses the growth of primary acute myeloid leukemia cells with IDH mutations. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,3,0 3.5.1.2 Leukemia, Myeloid, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27806325&form=6&db=m Inhibiting glutaminase in acute myeloid leukemia: metabolic dependency of selected AML subtypes. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Leukemia, Myeloid, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28947392&form=6&db=m Glutaminase inhibition improves FLT3 inhibitor therapy for acute myeloid leukemia. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Leukemia, Myeloid, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31387889&form=6&db=m Assessing Metabolic Intervention with a Glutaminase Inhibitor in Real-time by Hyperpolarized Magnetic Resonance in Acute Myeloid Leukemia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=943874&form=6&db=m [Enzymes participating in the formation of ammonia in various experimental liver diseases] diagnostic usage,ongoing research,unassigned 2,3,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15246207&form=6&db=m Intestinal glutaminase activity is increased in liver cirrhosis and correlates with minimal hepatic encephalopathy. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27696270&form=6&db=m New technologies - new insights into the pathogenesis of hepatic encephalopathy. causal interaction,unassigned 2,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27749985&form=6&db=m Validation study associating glutaminase promoter variations with hepatic encephalopathy in East Asian populations. diagnostic usage,ongoing research,therapeutic application,unassigned 4,4,1,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29305935&form=6&db=m Hedgehog-YAP Signaling Pathway Regulates Glutaminolysis to Control Activation of Hepatic Stellate Cells. causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32882667&form=6&db=m The role of WNT/?-catenin signaling pathway and glutamine metabolism in the pathogenesis of CCl4-induced liver fibrosis: Repositioning of niclosamide and concerns about lithium. ongoing research,unassigned 3,0 3.5.1.2 Liver Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24512823&form=6&db=m Ornithine phenylacetate targets alterations in the expression and activity of glutamine synthase and glutaminase to reduce ammonia levels in bile duct ligated rats. unassigned - 3.5.1.2 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24681885&form=6&db=m Circadian clock gene expression regulates cancer cell growth through glutaminase. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.5.1.2 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33016874&form=6&db=m A powerful drug combination strategy targeting glutamine addiction for the treatment of human liver cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25502225&form=6&db=m Mesenchymal phenotype predisposes lung cancer cells to impaired proliferation and redox stress in response to glutaminase inhibition. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26575584&form=6&db=m Inhibition of mitochondrial glutaminase activity reverses acquired erlotinib resistance in non-small cell lung cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27929535&form=6&db=m Dual targeting of glutaminase 1 and thymidylate synthase elicits death synergistically in NSCLC. causal interaction,unassigned 4,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28039459&form=6&db=m A novel glutaminase inhibitor-968 inhibits the migration and proliferation of non-small cell lung cancer cells by targeting EGFR/ERK signaling pathway. ongoing research,unassigned 2,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28099841&form=6&db=m Targeted Inhibition of EGFR and Glutaminase Induces Metabolic Crisis in EGFR Mutant Lung Cancer. causal interaction,ongoing research,therapeutic application,unassigned 4,3,3,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28871132&form=6&db=m An LC-MS Approach to Quantitative Measurement of Ammonia Isotopologues. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28967920&form=6&db=m Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis. causal interaction,ongoing research,therapeutic application,unassigned 1,2,3,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29515166&form=6&db=m Phosphorylation of glutaminase by PKC? is essential for its enzymatic activity and critically contributes to tumorigenesis. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30250881&form=6&db=m Dual targeting of EGFR and glutaminase in lung cancer. causal interaction,ongoing research,unassigned 4,2,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040157&form=6&db=m LKB1 and KEAP1/NRF2 Pathways Cooperatively Promote Metabolic Reprogramming with Enhanced Glutamine Dependence in KRAS-Mutant Lung Adenocarcinoma. causal interaction,unassigned 2,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31298457&form=6&db=m Inhibition of Anaplerotic Glutaminolysis Underlies Selenite Toxicity in Human Lung Cancer. ongoing research,unassigned 4,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32718002&form=6&db=m Glutaminase Inhibition on NSCLC Depends on Extracellular Alanine Exploitation. ongoing research,therapeutic application,unassigned 3,1,0 3.5.1.2 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33071215&form=6&db=m KEAP1/NFE2L2 Mutations Predict Lung Cancer Radiation Resistance That Can Be Targeted by Glutaminase Inhibition. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28185053&form=6&db=m Glutaminase expression is a poor prognostic factor in node-positive triple-negative breast cancer patients with a high level of tumor-infiltrating lymphocytes. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.5.1.2 Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19219026&form=6&db=m c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism. causal interaction,ongoing research,unassigned 1,3,0 3.5.1.2 Lymphoma, T-Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21854356&form=6&db=m Expanding Targets for a Metabolic Therapy of Cancer: L-Asparaginase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Malnutrition http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=496925&form=6&db=m Alterations in rat brain glutaminase and aldolase induced by lead ingestion following malnutrition. unassigned - 3.5.1.2 Malnutrition http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9292107&form=6&db=m Effect of protein malnutrition on the glycolytic and glutaminolytic enzyme activity of rat thymus and mesenteric lymph nodes. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12579526&form=6&db=m Human cutaneous melanoma expresses a significant phosphate-dependent glutaminase activity: a comparison with the surrounding skin of the same patient. causal interaction,diagnostic usage,ongoing research,unassigned 2,3,4,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17696751&form=6&db=m Modulation of metastatic potential of B16F10 melanoma cells by acivicin: synergistic action of alutaminase and potentiation of cisplatin cytotoxicity. diagnostic usage,unassigned 3,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29097210&form=6&db=m miR-137 inhibits glutamine catabolism and growth of malignant melanoma by targeting glutaminase. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30779126&form=6&db=m Long noncoding RNA OIP5-AS1 acts as a competing endogenous RNA to promote glutamine catabolism and malignant melanoma growth by sponging miR-217. causal interaction,diagnostic usage,unassigned 1,3,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30987979&form=6&db=m Concurrent Targeting of Glutaminolysis and Metabotropic Glutamate Receptor 1 (GRM1) Reduces Glutamate Bioavailability in GRM1+ Melanoma. causal interaction,unassigned 2,0 3.5.1.2 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33744390&form=6&db=m Expression of activated VEGFR2 by R1051Q mutation alters the energy metabolism of Sk-Mel-31 melanoma cells by increasing glutamine dependence. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.5.1.2 Memory Disorders http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22572473&form=6&db=m Curcumin Requires Tumor Necrosis Factor ? Signaling to Alleviate Cognitive Impairment Elicited by Lipopolysaccharide. diagnostic usage,ongoing research,unassigned 1,2,0 3.5.1.2 Meningioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34515312&form=6&db=m Glutamine anaplerosis is required for amino acid biosynthesis in human meningiomas. causal interaction,unassigned 4,0 3.5.1.2 Metabolic Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31734463&form=6&db=m Metabolic fingerprinting reveals extensive consequences of GLS hyperactivity. unassigned - 3.5.1.2 Mouth Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31324362&form=6&db=m c-Myc Overexpression Promotes Oral Cancer Cell Proliferation and Migration by Enhancing Glutaminase and Glutamine Synthetase Activity. ongoing research,therapeutic application,unassigned 4,1,0 3.5.1.2 Multiple Myeloma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28415782&form=6&db=m Glutaminase inhibitor CB-839 synergizes with carfilzomib in resistant multiple myeloma cells. ongoing research,therapeutic application,unassigned 1,1,0 3.5.1.2 Multiple Myeloma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29156762&form=6&db=m Glutaminase inhibition in multiple myeloma induces apoptosis causal interaction,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Multiple Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23850693&form=6&db=m Kinetic characterization of ebselen, chelerythrine and apomorphine as glutaminase inhibitors. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Multiple Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24269238&form=6&db=m Small molecule glutaminase inhibitors block glutamate release from stimulated microglia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26751560&form=6&db=m Glutaminase 2 is a novel negative regulator of small GTPase Rac1 and mediates p53 function in suppressing metastasis. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27725225&form=6&db=m Glutaminase 2 stabilizes Dicer to repress Snail and metastasis in hepatocellular carcinoma cells. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,3,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27829138&form=6&db=m Targeting Stromal Glutamine Synthetase in Tumors Disrupts Tumor Microenvironment-Regulated Cancer Cell Growth. ongoing research,unassigned 2,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28185053&form=6&db=m Glutaminase expression is a poor prognostic factor in node-positive triple-negative breast cancer patients with a high level of tumor-infiltrating lymphocytes. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30009389&form=6&db=m NRH:quinone oxidoreductase 2 (NQO2) and glutaminase (GLS) both play a role in large extracellular vesicles (LEV) formation in preclinical LNCaP-C4-2B prostate cancer model of progressive metastasis. ongoing research,unassigned 2,0 3.5.1.2 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33194749&form=6&db=m Targeting Glutaminolysis: New Perspectives to Understand Cancer Development and Novel Strategies for Potential Target Therapies. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=990468&form=6&db=m [Concentration of free glutamine and glutaminase activity in the gastric mucosa of patients with precancerous diseases and cancer of the stomach] diagnostic usage,ongoing research,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1287230&form=6&db=m Glutamine facilitates chemotherapy while reducing toxicity. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1341914&form=6&db=m Effect of aging on the glutaminase activity of neoplastic and immune tissues. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1346587&form=6&db=m Glutaminase and glutamine synthetase activities in human cirrhotic liver and hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1444793&form=6&db=m Effect of supplemental dietary glutamine on methotrexate concentrations in tumors. causal interaction,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1451103&form=6&db=m Investigation on glutamine amidohydrolase (EC 3.5.1.2) and glutamine aminotransferase (EC 2.5.1.15) activity in liver and plasma of EAC-bearing mice following glutaminase therapy. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,2,1 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1546896&form=6&db=m The effects of glutamine-enriched total parenteral nutrition on tumor growth and host tissues. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1675697&form=6&db=m Tumor regulation of hepatic glutamine metabolism. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1974167&form=6&db=m Short-term metabolic fate of L-[13N]glutamate in the Walker 256 carcinosarcoma in vivo. causal interaction,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2049779&form=6&db=m Investigation on phosphate dependent glutaminase (EC 3.5.1.2) activity in host tissues of EAC-bearing mice and response of liver EC 3.5.1.2 on Cu-ATP therapy. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2338817&form=6&db=m Glutamine-enriched diets support muscle glutamine metabolism without stimulating tumor growth. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2865980&form=6&db=m [13N]Ammonia and L-[amide-13N]glutamine metabolism in glutaminase-sensitive and glutaminase-resistant murine tumors. causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3342022&form=6&db=m Amino acid metabolism in tumour-bearing mice. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3801270&form=6&db=m Influence of reduced concentration of L-glutamine on growth and viability of cells in monolayer, in spheroids, and in experimental tumours. causal interaction,ongoing research,therapeutic application,unassigned 1,4,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4298788&form=6&db=m [Study of glutaminase and asparaginase activities in normal tissues and malignant tumors] causal interaction,diagnostic usage,ongoing research,unassigned 1,2,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4429959&form=6&db=m Properties and intracellular localization of Ehrlich ascites tumor cell glutaminase. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5126346&form=6&db=m [Effect of L-glutaminase from Pseudomonas aureofaciens in experimental tumors] ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5251291&form=6&db=m The proportionality of glutaminase content to growth rate and morphology of rat neoplasms. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5441084&form=6&db=m A series of transplantable rat mammary tumors with graded differentiation, growth rate, and glutaminase content. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5494007&form=6&db=m Studies on two types of glutaminase in normal and tumour bearing mice. ongoing research,therapeutic application,unassigned 4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5951788&form=6&db=m Studies on the mechanism of inhibition of tumor growth by the enzyme glutaminase. ongoing research,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6144677&form=6&db=m The pathways of glutamate and glutamine oxidation by tumor cell mitochondria. Role of mitochondrial NAD(P)+-dependent malic enzyme. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6794649&form=6&db=m Improvement in the persistence of microbial asparaginase and glutaminase in the circulation of the rat by chemical modifications. ongoing research,therapeutic application,unassigned 2,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7519362&form=6&db=m Cytokines decrease glutaminase expression in human fibroblasts. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7602720&form=6&db=m Harry M. Vars Research Award. Glutamine enhances immunoregulation of tumor growth. diagnostic usage,ongoing research,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7663171&form=6&db=m Tumor glutaminase purification. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7726679&form=6&db=m Glutamine enhances selectivity of chemotherapy through changes in glutathione metabolism. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7850545&form=6&db=m Decrease of glutaminase expression by interferon-gamma in human intestinal epithelial cells. causal interaction,diagnostic usage,ongoing research,unassigned 3,1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8099476&form=6&db=m Influence of progressive tumor growth on glutamine metabolism in skeletal muscle and kidney. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8137919&form=6&db=m Phosphate-activated glutaminase expression during tumor development. causal interaction,ongoing research,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8186431&form=6&db=m Anti-tumor efficacy of glutaminase-copper-ATP combination in mice bearing Ehrlich ascites carcinoma. causal interaction,therapeutic application,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8490566&form=6&db=m Effects of various dietary fatty acids on enzyme activities of carbohydrate and glutamine metabolism and the metabolic response of lymphocytes and macrophages during Walker-256 ascites cell tumour growth in rats. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9042341&form=6&db=m Submitochondrial localization and membrane topography of Ehrlich ascitic tumour cell glutaminase. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9202643&form=6&db=m Hepatic glutaminase gene expression in the tumor-bearing rat. diagnostic usage,ongoing research,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9920404&form=6&db=m Involvement of essential cysteine and histidine residues in the activity of isolated glutaminase from tumour cells. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9929166&form=6&db=m Early differential expression of two glutaminase mRNAs in mouse spleen after tumor implantation. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10587609&form=6&db=m Cholesterol inhibits glutamine metabolism in LLC WRC256 tumour cells but does not affect it in lymphocytes: possible implications for tumour cell proliferation. diagnostic usage,ongoing research,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10607927&form=6&db=m Angiogenesis a putative new approach in glutamine related therapy. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10620514&form=6&db=m Molecular cloning, sequencing and expression studies of the human breast cancer cell glutaminase. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10746973&form=6&db=m Isolation and purification of phosphate dependent glutaminase from sarcoma-180 tumor and its antineoplastic effects on murine model system. ongoing research,therapeutic application,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10816417&form=6&db=m Inhibition of glutaminase expression by antisense mRNA decreases growth and tumourigenicity of tumour cells. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10928057&form=6&db=m Changes in mRNAs for enzymes of glutamine metabolism in the tumor-bearing mouse. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10965812&form=6&db=m A general survey of glutamine level in different tissues of murine solid tumor bearing mice before and after therapy with purified glutaminase. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11063916&form=6&db=m Mitochondrial glutathione depletion by glutamine in growing tumor cells. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11169963&form=6&db=m Ehrlich ascites tumor cells expressing anti-sense glutaminase mRNA lose their capacity to evade the mouse immune system. causal interaction,ongoing research,therapeutic application,unassigned 4,3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11233093&form=6&db=m Neovascularisation offers a new perspective to glutamine related therapy. causal interaction,ongoing research,therapeutic application,unassigned 1,4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11876557&form=6&db=m Effect of purified glutaminase from human ascites fluid on experimental tumor bearing mice. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,4,3 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=13344809&form=6&db=m Changes in the glutaminase activity of liver tissue from rats during the development of hepatic tumors by carcinogen feeding. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14195348&form=6&db=m EFFECT OF ADMINISTRATION OF THE ENZYME GLUTAMINASE ON THE GROWTH OF CANCER CELLS. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15496140&form=6&db=m Co-expression of glutaminase K and L isoenzymes in human tumour cells. causal interaction,ongoing research,therapeutic application,unassigned 1,4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15511236&form=6&db=m Antisense glutaminase inhibition decreases glutathione antioxidant capacity and increases apoptosis in Ehrlich ascitic tumour cells. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15639344&form=6&db=m Inhibition of glutaminase expression increases Sp1 phosphorylation and Sp1/Sp3 transcriptional activity in Ehrlich tumor cells. causal interaction,ongoing research,therapeutic application,unassigned 2,4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15850218&form=6&db=m [The regulatory action of dipeptide "Deglutam" on the glutamine metabolized enzymes in the carcinosarcoma SM-1 cells] ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16101144&form=6&db=m Sensitisation of Ehrlich ascitic tumour cells to methotrexate by inhibiting glutaminase. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16263711&form=6&db=m Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor necrosis factor-alpha and chemotherapy. ongoing research,therapeutic application,unassigned 3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16294018&form=6&db=m Identification of genes downregulated in tumor cells expressing antisense glutaminase mRNA by differential display. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17696751&form=6&db=m Modulation of metastatic potential of B16F10 melanoma cells by acivicin: synergistic action of alutaminase and potentiation of cisplatin cytotoxicity. diagnostic usage,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17940881&form=6&db=m Relative expression of mRNAS coding for glutaminase isoforms in CNS tissues and CNS tumors. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18584486&form=6&db=m Glutamine affects glutathione recycling enzymes in a DMBA-induced breast cancer model. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18678946&form=6&db=m Expression, purification and crystallization of Helicobacter pylori L-asparaginase. diagnostic usage,therapeutic application,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18690705&form=6&db=m Probing the structure and function of human glutaminase-interacting protein: a possible target for drug design. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19428809&form=6&db=m Glutamine in neoplastic cells: focus on the expression and roles of glutaminases. causal interaction,ongoing research,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19703661&form=6&db=m Glutamine homeostasis and mitochondrial dynamics. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19806017&form=6&db=m MYC, microRNAs and glutamine addiction in cancers. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20863288&form=6&db=m Imaging tumour cell metabolism using hyperpolarized 13C magnetic resonance spectroscopy. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21234284&form=6&db=m Glutaminase: a hot spot for regulation of cancer cell metabolism? causal interaction,diagnostic usage,unassigned 4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21417405&form=6&db=m Promiscuous Binding at the Crossroads of Numerous Cancer Pathways: Insight from the Binding of Glutaminase Interacting Protein with Glutaminase L. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21787750&form=6&db=m Identification of brain-specific angiogenesis inhibitor 2 as an interaction partner of glutaminase interacting protein. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21854356&form=6&db=m Expanding Targets for a Metabolic Therapy of Cancer: L-Asparaginase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21960526&form=6&db=m Therapeutic Targeting of Myc-Reprogrammed Cancer Cell Metabolism. causal interaction,therapeutic application,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21999665&form=6&db=m BPTES inhibition of hGA(124-551), a truncated form of human kidney-type glutaminase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22144112&form=6&db=m Glutamate released by Japanese encephalitis virus-infected microglia involves TNF-? signaling and contributes to neuronal death. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22225880&form=6&db=m Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells. causal interaction,therapeutic application,unassigned 4,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22228304&form=6&db=m Mitochondrial localization and structure-based phosphate activation mechanism of Glutaminase C with implications for cancer metabolism. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22326218&form=6&db=m The metabolic profile of tumors depends on both the responsible genetic lesion and tissue type. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22496480&form=6&db=m Dibenzophenanthridines as inhibitors of glutaminase C and cancer cell proliferation. causal interaction,ongoing research,therapeutic application,unassigned 4,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22538822&form=6&db=m Structural basis for the allosteric inhibitory mechanism of human kidney-type glutaminase (KGA) and its regulation by Raf-Mek-Erk signaling in cancer cell metabolism. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22570721&form=6&db=m Selection of metastatic breast cancer cells based on adaptability of their metabolic state. diagnostic usage,ongoing research,unassigned 3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22615405&form=6&db=m Reprogramming of proline and glutamine metabolism contributes to the proliferative and metabolic responses regulated by oncogenic transcription factor c-MYC. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22634383&form=6&db=m The NF-?B member p65 controls glutamine metabolism through miR-23a. causal interaction,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22679499&form=6&db=m Mammalian glutaminase Gls2 gene encodes two functional alternative transcripts by a surrogate promoter usage mechanism. causal interaction,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22934847&form=6&db=m Glutaminase Isoenzymes as Key Regulators in Metabolic and Oxidative Stress against Cancer. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23219172&form=6&db=m Rho GTPases and their roles in cancer metabolism. ongoing research,therapeutic application,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23470539&form=6&db=m Targeting cellular metabolism to improve cancer therapeutics. causal interaction,ongoing research,therapeutic application,unassigned 2,1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23507704&form=6&db=m Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer. diagnostic usage,ongoing research,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23574722&form=6&db=m p63 regulates glutaminase 2 expression. ongoing research,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23689113&form=6&db=m In vivo and in vitro liver cancer metabolism observed with hyperpolarized [5-(13)C]glutamine. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,4,1 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23722553&form=6&db=m Evaluation of LDH-A and glutaminase inhibition in vivo by hyperpolarized 13C-pyruvate magnetic resonance spectroscopy of tumors. therapeutic application,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23850693&form=6&db=m Kinetic characterization of ebselen, chelerythrine and apomorphine as glutaminase inhibitors. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23921958&form=6&db=m Multifunctional antitumor molecule 5'-triphosphate siRNA combining glutaminase silencing and RIG-I activation. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24047273&form=6&db=m Therapeutic strategies impacting cancer cell glutamine metabolism. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24091747&form=6&db=m Cancer cell metabolism: implications for therapeutic targets. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24098668&form=6&db=m Small Angle X-Ray Scattering Studies of Mitochondrial Glutaminase C Reveal Extended Flexible Regions, and Link Oligomeric State with Enzyme Activity. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24140288&form=6&db=m Glutaminase regulation in cancer cells: a druggable chain of events. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24269238&form=6&db=m Small molecule glutaminase inhibitors block glutamate release from stimulated microglia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24276018&form=6&db=m Both GLS silencing and GLS2 overexpression synergize with oxidative stress against proliferation of glioma cells. ongoing research,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24316975&form=6&db=m MYC-driven accumulation of 2-hydroxyglutarate is associated with breast cancer prognosis. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24451979&form=6&db=m Structural basis for the active site inhibition mechanism of human kidney-type glutaminase (KGA). causal interaction,therapeutic application,unassigned 1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24659632&form=6&db=m The glutaminase activity of L-asparaginase is not required for anticancer activity against ASNS-negative cells. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24681885&form=6&db=m Circadian clock gene expression regulates cancer cell growth through glutaminase. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24797434&form=6&db=m Glutaminase 2 negatively regulates the PI3K/AKT signaling and shows tumor suppression activity in human hepatocellular carcinoma. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25026281&form=6&db=m Discovery of selective inhibitors of Glutaminase-2, which inhibit mTORC1, activate autophagy and inhibit proliferation in cancer cells. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25085245&form=6&db=m The SIRT1/HIF2? axis drives reductive glutamine metabolism under chronic acidosis and alters tumor response to therapy. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25237859&form=6&db=m Action at a distance: allostery and the development of drugs to target cancer cell metabolism. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25274019&form=6&db=m Novel glutaminase free L-asparaginase from Nocardiopsis alba NIOT-VKMA08: production, optimization, functional and molecular characterization. ongoing research,therapeutic application,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25337608&form=6&db=m Characterisation and molecular dynamic simulations of J15 asparaginase from Photobacterium sp. strain J15. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25409906&form=6&db=m Dynamic analyses of alternative polyadenylation from RNA-seq reveal a 3'-UTR landscape across seven tumour types. therapeutic application,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25424834&form=6&db=m PEG-PHB-glutaminase nanoparticle inhibits cancer cell proliferation in vitro through glutamine deprivation. causal interaction,ongoing research,therapeutic application,unassigned 1,3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25426679&form=6&db=m Simultaneously targeting tissue transglutaminase and kidney type glutaminase sensitizes cancer cells to acid toxicity and offers new opportunities for therapeutic intervention. causal interaction,ongoing research,therapeutic application,unassigned 3,1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25502225&form=6&db=m Mesenchymal phenotype predisposes lung cancer cells to impaired proliferation and redox stress in response to glutaminase inhibition. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25524627&form=6&db=m Synthetic lethality of combined glutaminase and Hsp90 inhibition in mTORC1-driven tumor cells. therapeutic application,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25548170&form=6&db=m Mechanism by which a recently discovered allosteric inhibitor blocks glutamine metabolism in transformed cells. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25663193&form=6&db=m Glutaminolysis and carcinogenesis of oral squamous cell carcinoma. diagnostic usage,ongoing research,therapeutic application,unassigned 1,2,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25837287&form=6&db=m Glutaminases in brain: Multiple isoforms for many purposes. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25915584&form=6&db=m Targeted inhibition of tumor-specific glutaminase diminishes cell-autonomous tumorigenesis. causal interaction,therapeutic application,unassigned 2,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26564960&form=6&db=m Q-ing tumor glutaminase for therapy. causal interaction,therapeutic application,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26581715&form=6&db=m Glutaminases in slowly proliferating gastroenteropancreatic neuroendocrine neoplasms/tumors (GEP-NETs): Selective overexpression of mRNA coding for the KGA isoform. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26691453&form=6&db=m Kinetic properties of Streptomyces canarius L- Glutaminase and its anticancer efficiency. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26751681&form=6&db=m Replication of the Shrimp Virus WSSV Depends on Glutamate-Driven Anaplerosis. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26833123&form=6&db=m The Ephrin-A1/EPHA2 Signaling Axis Regulates Glutamine Metabolism in HER2-Positive Breast Cancer. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26985303&form=6&db=m Glutaminase GLS1 Inhibitors as Potential Cancer Treatment. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27157265&form=6&db=m TUMOUR-DERIVED GLUTAMATE: LINKING ABERRANT CANCER CELL METABOLISM TO PERIPHERAL SENSORY PAIN PATHWAYS. causal interaction,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27330530&form=6&db=m The potential of halophilic and halotolerant bacteria for the production of antineoplastic enzymes: L-asparaginase and L-glutaminase. causal interaction,therapeutic application,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27338638&form=6&db=m Glutaminase 1 inhibition reduces thymidine synthesis in NSCLC. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27542409&form=6&db=m Mechanistic Basis of Glutaminase Activation: A Key Enzyme that Promotes Glutamine Metabolism in Cancer Cells. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27559084&form=6&db=m Combination therapy with BPTES nanoparticles and metformin targets the metabolic heterogeneity of pancreatic cancer. causal interaction,ongoing research,therapeutic application,unassigned 4,1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27582590&form=6&db=m In Silico Analysis of Glutaminase from Different Species of Escherichia and Bacillus. therapeutic application,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27725225&form=6&db=m Glutaminase 2 stabilizes Dicer to repress Snail and metastasis in hepatocellular carcinoma cells. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27806325&form=6&db=m Inhibiting glutaminase in acute myeloid leukemia: metabolic dependency of selected AML subtypes. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27829138&form=6&db=m Targeting Stromal Glutamine Synthetase in Tumors Disrupts Tumor Microenvironment-Regulated Cancer Cell Growth. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27885632&form=6&db=m Glutamine Metabolism in Gliomas. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27913195&form=6&db=m Breast cancer-derived extracellular vesicles stimulate myofibroblast differentiation and pro-angiogenic behavior of adipose stem cells. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28039459&form=6&db=m A novel glutaminase inhibitor-968 inhibits the migration and proliferation of non-small cell lung cancer cells by targeting EGFR/ERK signaling pathway. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28122247&form=6&db=m Arginine Deprivation Inhibits the Warburg Effect and Upregulates Glutamine Anaplerosis and Serine Biosynthesis in ASS1-Deficient Cancers. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28168879&form=6&db=m Head and Neck Squamous Cell Carcinoma Metabolism Draws on Glutaminolysis, and Stemness Is Specifically Regulated by Glutaminolysis via Aldehyde Dehydrogenase. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28174105&form=6&db=m Physapubescin, a natural withanolide as a kidney-type glutaminase (KGA) inhibitor. causal interaction,therapeutic application,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28174256&form=6&db=m A Time for MYC: Metabolism and Therapy. causal interaction,therapeutic application,unassigned 1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28185053&form=6&db=m Glutaminase expression is a poor prognostic factor in node-positive triple-negative breast cancer patients with a high level of tumor-infiltrating lymphocytes. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28196863&form=6&db=m Conformational Changes in the Activation Loop of Mitochondrial Glutaminase C: A Direct Fluorescence Read-Out that Distinguishes the Binding of Allosteric Inhibitors from Activators. causal interaction,diagnostic usage,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28208301&form=6&db=m Biomolecular Interaction Assays Identified Dual Inhibitors of Glutaminase and Glutamate Dehydrogenase That Disrupt Mitochondrial Function and Prevent Growth of Cancer Cells. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28462847&form=6&db=m Breaking the ritual metabolic cycle in order to save acetyl CoA: A potential role for mitochondrial humanin in T2 bladder cancer aggressiveness. diagnostic usage,ongoing research,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28526749&form=6&db=m The origin and evolution of human glutaminases and their atypical C-terminal ankyrin repeats. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28611197&form=6&db=m Treatment of Pancreatic Cancer Patient-Derived Xenograft Panel with Metabolic Inhibitors Reveals Efficacy of Phenformin. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28627692&form=6&db=m The role of intestinal endotoxemia in a rat model of aluminum neurotoxicity. diagnostic usage,ongoing research,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28811348&form=6&db=m A Critical Role of Glutamine and Asparagine ?-Nitrogen in Nucleotide Biosynthesis in Cancer Cells Hijacked by an Oncogenic Virus. ongoing research,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28826492&form=6&db=m Environmental cystine drives glutamine anaplerosis and sensitizes cancer cells to glutaminase inhibition. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28967920&form=6&db=m Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis. causal interaction,ongoing research,therapeutic application,unassigned 1,2,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28978620&form=6&db=m therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29097210&form=6&db=m miR-137 inhibits glutamine catabolism and growth of malignant melanoma by targeting glutaminase. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29107960&form=6&db=m Glutamine deficiency induces DNA alkylation damage and sensitizes cancer cells to alkylating agents through inhibition of ALKBH enzymes. therapeutic application,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29208682&form=6&db=m The receptor tyrosine kinase EphA2 promotes glutamine metabolism in tumors by activating the transcriptional coactivators YAP and TAZ. causal interaction,ongoing research,therapeutic application,unassigned 1,1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29212209&form=6&db=m Targeted inhibition of glutaminase as a potential new approach for the treatment of causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29266697&form=6&db=m Expression of the glutamine metabolism-related proteins glutaminase 1 and glutamate dehydrogenase in canine mammary tumours. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29317493&form=6&db=m Characterization of the interactions of potent allosteric inhibitors with glutaminase C, a key enzyme in cancer cell glutamine metabolism. therapeutic application,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29371926&form=6&db=m A natural inhibitor of kidney-type glutaminase: a withanolide from therapeutic application,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29420817&form=6&db=m Glutamine metabolism via glutaminase 1 in autosomal-dominant polycystic kidney disease. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29515166&form=6&db=m Phosphorylation of glutaminase by PKC? is essential for its enzymatic activity and critically contributes to tumorigenesis. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29576625&form=6&db=m Targeting glutaminolysis in chondrosarcoma in context of the IDH1/2 mutation. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29633308&form=6&db=m Molecular targeting of glutaminase sensitizes ovarian cancer cells to chemotherapy. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,3,4 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29715600&form=6&db=m Caudatan A, an undescribed human kidney-type glutaminase inhibitor with tetracyclic flavan from Ohwia caudata. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29763620&form=6&db=m Targeting Therapy Resistance: When Glutamine Catabolism Becomes Essential. causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29763624&form=6&db=m The GSK3 Signaling Axis Regulates Adaptive Glutamine Metabolism in Lung Squamous Cell Carcinoma. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29788892&form=6&db=m Inhibition of Glycolysis and Glutaminolysis: An Emerging Drug Discovery Approach to Combat Cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29793408&form=6&db=m Recent Development of Small Molecule Glutaminase Inhibitors. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29868609&form=6&db=m A Metabolomics Study of BPTES Altered Metabolism in Human Breast Cancer Cell Lines. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29958416&form=6&db=m Caffeic Acid Targets AMPK Signaling and Regulates Tricarboxylic Acid Cycle Anaplerosis while Metformin Downregulates HIF-1?-Induced Glycolytic Enzymes in Human Cervical Squamous Cell Carcinoma Lines. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30053497&form=6&db=m Glutaminase isoenzymes in the metabolic therapy of cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,2,4 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30072394&form=6&db=m Glutamate-Weighted Chemical Exchange Saturation Transfer Magnetic Resonance Imaging Detects Glutaminase Inhibition in a Mouse Model of Triple-Negative Breast Cancer. therapeutic application,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30092248&form=6&db=m N-terminal phosphorylation of glutaminase C decreases its enzymatic activity and cancer cell migration. diagnostic usage,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30122555&form=6&db=m Cytosolic Aspartate Availability Determines Cell Survival When Glutamine Is Limiting. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30193917&form=6&db=m Selective reduction in glutaminase activity of l?Asparaginase by asparagine 248 to serine mutation: A combined computational and experimental effort in blood cancer treatment. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30250881&form=6&db=m Dual targeting of EGFR and glutaminase in lung cancer. causal interaction,ongoing research,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30273516&form=6&db=m Glutaminase inhibitors: a patent review. causal interaction,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30458442&form=6&db=m miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30543285&form=6&db=m Novel 1,3,4-Selenadiazole Containing Kidney-Type Glutaminase Inhibitors Showed Improved Cellular Uptake and Antitumor Activity. causal interaction,therapeutic application,unassigned 3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30557074&form=6&db=m Glutaminase Inhibitor CB-839 Increases Radiation Sensitivity of Lung Tumor Cells and Human Lung Tumor Xenografts in Mice. ongoing research,therapeutic application,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30646605&form=6&db=m Metformin Impairs Glutamine Metabolism and Autophagy in Tumour Cells. causal interaction,therapeutic application,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30674873&form=6&db=m Glutaminase 1 expression in colorectal cancer cells is induced by hypoxia and required for tumor growth, invasion, and metastatic colonization. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30786811&form=6&db=m The HGF-MET axis coordinates liver cancer metabolism and autophagy for chemotherapeutic resistance. diagnostic usage,therapeutic application,unassigned 1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30796006&form=6&db=m LncRNA EPB41L4A-AS1 regulates glycolysis and glutaminolysis by mediating nucleolar translocation of HDAC2. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30871151&form=6&db=m Multiomics Analysis Reveals that GLS and GLS2 Differentially Modulate the Clinical Outcomes of Cancer. causal interaction,therapeutic application,unassigned 2,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30936077&form=6&db=m Several Faces of Glutaminase Regulation in Cells. therapeutic application,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30970252&form=6&db=m Uncovering the Role of N-Acetyl-Aspartyl-Glutamate as a Glutamate Reservoir in Cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30993582&form=6&db=m Isolation and screening of extracellular anticancer enzymes from halophilic and halotolerant bacteria from different saline environments in Iran. diagnostic usage,ongoing research,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31038055&form=6&db=m Metabolic reprogramming of cancer by chemicals that target glutaminase isoenzymes. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040157&form=6&db=m LKB1 and KEAP1/NRF2 Pathways Cooperatively Promote Metabolic Reprogramming with Enhanced Glutamine Dependence in KRAS-Mutant Lung Adenocarcinoma. causal interaction,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040181&form=6&db=m Dual inhibition of glutaminase and carnitine palmitoyltransferase decreases growth and migration of glutaminase inhibition-resistant triple-negative breast cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,3,3 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31088535&form=6&db=m Glutamine to proline conversion is associated with response to glutaminase inhibition in breast cancer. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31100352&form=6&db=m Therapeutic targeting of glutaminolysis as an essential strategy to combat cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31139406&form=6&db=m Isocitrate dehydrogenase 1-mutated cancers are sensitive to the green tea polyphenol epigallocatechin-3-gallate. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31189611&form=6&db=m Targeting Mitochondrial Proline Dehydrogenase with a Suicide Inhibitor to Exploit Synthetic Lethal Interactions with p53 Upregulation and Glutaminase Inhibition. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31196962&form=6&db=m Inhibition of GLS suppresses proliferation and promotes apoptosis in prostate cancer. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31199640&form=6&db=m Discovery of a Thiadiazole-Pyridazine-Based Allosteric Glutaminase 1 Inhibitor Series That Demonstrates Oral Bioavailability and Activity in Tumor Xenograft Models. therapeutic application,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31209181&form=6&db=m Glutaminase Activity of L-Asparaginase Contributes to Durable Preclinical Activity against Acute Lymphoblastic Leukemia. diagnostic usage,ongoing research,therapeutic application,unassigned 1,3,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31211239&form=6&db=m Glutamine addiction: an Achilles heel in esophageal cancers with dysregulation of CDK4/6. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31231915&form=6&db=m Upregulation of the Glutaminase II Pathway Contributes to Glutamate Production upon Glutaminase 1 Inhibition in Pancreatic Cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31257527&form=6&db=m Expression of GLS1 in intrahepatic cholangiocarcinoma and its clinical significance. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31303578&form=6&db=m Inhibition of Glucose Transporters and Glutaminase Synergistically Impairs Tumor Cell Growth. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31324362&form=6&db=m c-Myc Overexpression Promotes Oral Cancer Cell Proliferation and Migration by Enhancing Glutaminase and Glutamine Synthetase Activity. ongoing research,therapeutic application,unassigned 4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31387889&form=6&db=m Assessing Metabolic Intervention with a Glutaminase Inhibitor in Real-time by Hyperpolarized Magnetic Resonance in Acute Myeloid Leukemia. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31387898&form=6&db=m Immunosuppressive Immature Myeloid Cell Generation Is Controlled by Glutamine Metabolism in Human Cancer. causal interaction,therapeutic application,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31449760&form=6&db=m Defining and targeting wild-type BRCA high-grade serous ovarian cancer: DNA repair and cell cycle checkpoints. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31465967&form=6&db=m Physapubescin I from husk tomato suppresses SW1990 cancer cell growth by targeting kidney-type glutaminase. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31474484&form=6&db=m GAC inhibitors with a 4-hydroxypiperidine spacer: Requirements for potency. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31539503&form=6&db=m Starving the Devourer: Cutting Cancer Off from Its Favorite Foods. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31541193&form=6&db=m GLS2 is protumorigenic in breast cancers. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31571981&form=6&db=m Effect of glutaminase inhibition on cancer-induced bone pain. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31574293&form=6&db=m Dysregulation of glutaminase and glutamine synthetase in cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 4,2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31577957&form=6&db=m Liver-Type Glutaminase GLS2 Is a Druggable Metabolic Node in Luminal-Subtype Breast Cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31596504&form=6&db=m The role of glutaminase in cancer. causal interaction,ongoing research,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31601700&form=6&db=m Pharmacokinetic Assessment of 18F-(2S,4R)-4-Fluoroglutamine in Patients with Cancer. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31603674&form=6&db=m Development and Characterization of a Fluorescent Probe for GLS1 and the Application for High-Throughput Screening of Allosteric Inhibitors. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31668020&form=6&db=m Glucose and glutamine metabolism in relation to mutational status in NSCLC histological subtypes. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31743703&form=6&db=m Purification and characterization of l-glutaminase enzyme from camel liver: Enzymatic anticancer property. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,4 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31813821&form=6&db=m Activation of Oxidative Stress Response in Cancer Generates a Druggable Dependency on Exogenous Non-essential Amino Acids. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31843902&form=6&db=m SIRT5 stabilizes mitochondrial glutaminase and supports breast cancer tumorigenesis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,2 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31846380&form=6&db=m Production, optimization, purification, characterization, and anti-cancer application of extracellular L-glutaminase produced from the marine bacterial isolate. ongoing research,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31866300&form=6&db=m Glutamine Skipping the Q into Mitochondria. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31871054&form=6&db=m The activation loop and substrate-binding cleft of glutaminase C are allosterically coupled. causal interaction,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31899205&form=6&db=m OGDHL silencing promotes hepatocellular carcinoma by reprogramming glutamine metabolism. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,2,4 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32042057&form=6&db=m Nuclear Translocation of Glutaminase GLS2 in Human Cancer Cells Associates with Proliferation Arrest and Differentiation. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32057283&form=6&db=m Patents targeting the Warburg effect for cancer therapy: an interview with William P Katt. causal interaction,therapeutic application,unassigned 1,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32150977&form=6&db=m Glutaminases as a Novel Target for SDHB-Associated Pheochromocytomas/Paragangliomas. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32158544&form=6&db=m Glutaminase-1 (GLS1) inhibition limits metastatic progression in osteosarcoma. causal interaction,therapeutic application,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32206103&form=6&db=m Metabolic remodeling by TIGAR overexpression is a therapeutic target in esophageal squamous-cell carcinoma. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32218849&form=6&db=m Intratumoral heterogeneity of glutaminase and lactate dehydrogenase A protein expression in colorectal cancer. causal interaction,diagnostic usage,unassigned 1,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32219214&form=6&db=m Kidney-Type Glutaminase Inhibitor Hexylselen Selectively Kills Cancer Cells via a Three-Pronged Mechanism. therapeutic application,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32328963&form=6&db=m Molecular modeling and LC-MS-based metabolomics of a glutamine-valproic acid (Gln-VPA) derivative on HeLa cells. causal interaction,ongoing research,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32337072&form=6&db=m A comparative pharmaco-metabolomic study of glutaminase inhibitors in glioma stem-like cells confirms biological effectiveness but reveals differences in target-specificity. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32401642&form=6&db=m Autophagy in the physiological endometrium and cancer. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32624705&form=6&db=m Palbociclib treatment alters nucleotide biosynthesis and glutamine dependency in A549 cells. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32681190&form=6&db=m Glutaminases regulate glutathione and oxidative stress in cancer. diagnostic usage,therapeutic application,unassigned 1,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32691018&form=6&db=m NRF2 activation promotes the recurrence of dormant tumour cells through regulation of redox and nucleotide metabolism. causal interaction,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32694609&form=6&db=m Identifying strategies to target the metabolic flexibility of tumours. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32695682&form=6&db=m Metabolic and OXPHOS Activities Quantified by Temporal ex vivo Analysis Display Patient-Specific Metabolic Vulnerabilities in Human Breast Cancers. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32718002&form=6&db=m Glutaminase Inhibition on NSCLC Depends on Extracellular Alanine Exploitation. ongoing research,therapeutic application,unassigned 3,1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32726986&form=6&db=m Erratum: Majewska, E. et al. Transfection with GLS2 Glutaminase (GAB) Sensitizes Human Glioblastoma Cell Lines to Oxidative Stress by a Common Mechanism Involving Suppression of the PI3K/AKT Pathway. Cancers 2019, 11, 115. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32859605&form=6&db=m Inhibition of the MYC-regulated glutaminase metabolic axis is an effective synthetic lethal approach for treating chemoresistant cancers. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32863227&form=6&db=m Metabolic reprogramming sustains cancer cell survival following extracellular matrix detachment. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33004309&form=6&db=m A facile and sensitive method of quantifying glutaminase binding to its inhibitor CB-839 in tissues. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,3 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33005401&form=6&db=m Disruption of redox homeostasis for combinatorial drug efficacy in K-Ras tumors as revealed by metabolic connectivity profiling. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33087507&form=6&db=m Glutaminase Inhibitors Induce Thiol-Mediated Oxidative Stress and Radiosensitization in Treatment-Resistant Cervical Cancers. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33118821&form=6&db=m Discovery of IPN60090, a Clinical Stage Selective Glutaminase-1 (GLS-1) Inhibitor with Excellent Pharmacokinetic and Physicochemical Properties. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33179520&form=6&db=m Upregulation of glutaminase 2 and neutrophil cytosolic factor 2 is associated with the poor prognosis of glioblastoma. causal interaction,diagnostic usage,unassigned 4,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33194749&form=6&db=m Targeting Glutaminolysis: New Perspectives to Understand Cancer Development and Novel Strategies for Potential Target Therapies. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33207079&form=6&db=m HRD1 inhibits fatty acid oxidation and tumorigenesis by ubiquitinating CPT2 in triple-negative breast cancer. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33229301&form=6&db=m Phase 1 Trial of MLN0128 (Sapanisertib) and CB-839 HCl (Telaglenastat) in Patients With Advanced NSCLC (NCI 10327): Rationale and Study Design. therapeutic application,unassigned 4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33229340&form=6&db=m Glutamine-Directed Migration of Cancer-Activated Fibroblasts Facilitates Epithelial Tumor Invasion. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33320840&form=6&db=m Selective glutamine metabolism inhibition in tumor cells improves antitumor T lymphocyte activity in triple-negative breast cancer. causal interaction,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33323404&form=6&db=m STK11/LKB1 Mutations in NSCLC Are Associated with KEAP1/NRF2-Dependent Radiotherapy Resistance Targetable by Glutaminase Inhibition. unassigned - 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33389217&form=6&db=m Purification, characterization, and anticancer and antioxidant activities of L-glutaminase from Aspergillus versicolor Faesay4. ongoing research,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33397990&form=6&db=m Author Correction: Nuclear Translocation of Glutaminase GLS2 in Human Cancer Cells Associates with Proliferation Arrest and Differentiation. ongoing research,unassigned 2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33450358&form=6&db=m Glutaminase inhibition with telaglenastat (CB-839) improves treatment response in combination with ionizing radiation in head and neck squamous cell carcinoma models. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33510635&form=6&db=m Amino Acid Degrading Enzymes and Autophagy in Cancer Therapy. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33610185&form=6&db=m Glutaminase isoforms expression switches microRNA levels and oxidative status in glioblastoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,1 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33753479&form=6&db=m A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33792311&form=6&db=m Structure-Enabled Discovery of Novel Macrocyclic Inhibitors Targeting Glutaminase 1 Allosteric Binding Site. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33807313&form=6&db=m L-Glutaminase Synthesis by Marine Halomonas meridiana Isolated from the Red Sea and Its Efficiency against Colorectal Cancer Cell Lines. ongoing research,therapeutic application,unassigned 2,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33816218&form=6&db=m Effect of He Plasma Jet Versus Surface Plasma on the Metabolites of Acute Myeloid Leukemia Cells. causal interaction,diagnostic usage,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33910646&form=6&db=m Glutaminolysis dynamics during astrocytoma progression correlates with tumor aggressiveness. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33947068&form=6&db=m Evaluation of Glutaminase Expression in Prostate Adenocarcinoma and Correlation with Clinicopathologic Parameters. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33966211&form=6&db=m Impact of Acidosis-Regulated MicroRNAs on the Expression of Their Target Genes in Experimental Tumors In Vivo. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33991485&form=6&db=m SUCLA2-coupled regulation of GLS succinylation and activity counteracts oxidative stress in tumor cells. ongoing research,unassigned 1,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34014548&form=6&db=m Metabolic Intersection of Cancer and Cardiovascular Diseases: Opportunities for Cancer Therapy. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34085048&form=6&db=m Targeting glutamine dependence through GLS1 inhibition suppresses ARID1A-inactivated clear cell ovarian carcinoma. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34119480&form=6&db=m GLS1 depletion inhibited colorectal cancer proliferation and migration via redox/Nrf2/autophagy-dependent pathway. causal interaction,unassigned 3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34172075&form=6&db=m Impaired anaplerosis is a major contributor to glycolysis inhibitor toxicity in glioma. causal interaction,ongoing research,therapeutic application,unassigned 1,3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34285061&form=6&db=m A Phase I Dose-Escalation and Expansion Study of Telaglenastat in Patients with Advanced or Metastatic Solid Tumors. ongoing research,therapeutic application,unassigned 3,3,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34354052&form=6&db=m Compound 968 reverses adriamycin resistance in breast cancer MCF-7ADR cells via inhibiting P-glycoprotein function independently of glutaminase. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34486482&form=6&db=m Targeting glutamine metabolism and autophagy: the combination for prostate cancer radiosensitization. unassigned - 3.5.1.2 Nephritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5038304&form=6&db=m [Glutaminase activity of rat kidney tissue in experimental nephritis] ongoing research,unassigned 4,0 3.5.1.2 Nephrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4446023&form=6&db=m Glutaminase activity in the kidney of experimental nephrosis. ongoing research,therapeutic application,unassigned 4,1,0 3.5.1.2 Neural Tube Defects http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32636743&form=6&db=m Altered Glutaminase 1 Activity During Neurulation and Its Potential Implications in Neural Tube Defects. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18274897&form=6&db=m Novel form of phosphate activated glutaminase in cultured astrocytes and human neuroblastoma cells, PAG in brain pathology and localization in the mitochondria. ongoing research,unassigned 4,0 3.5.1.2 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19894115&form=6&db=m Kinetics of a Novel Isoform of Phosphate Activated Glutaminase (PAG) in SH-SY5Y Neuroblastoma Cells. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,2,0 3.5.1.2 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26528759&form=6&db=m Myc promotes glutaminolysis in human neuroblastoma through direct activation of glutaminase 2. causal interaction,ongoing research,unassigned 1,2,0 3.5.1.2 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28800318&form=6&db=m MiR-513c suppresses neuroblastoma cell migration, invasion, and proliferation through direct targeting glutaminase (GLS). causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 3.5.1.2 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11458996&form=6&db=m Unaltered cytochrome oxidase, glutamate dehydrogenase and glutaminase activities in platelets from patients with sporadic amyotrophic lateral sclerosis--a study of potential pathogenetic mechanisms in neurodegenerative diseases. unassigned - 3.5.1.2 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18059978&form=6&db=m Potentiation of Excitotoxicity in HIV-1 Associated Dementia and the Significance of Glutaminase. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,1,0 3.5.1.2 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23578284&form=6&db=m IL-1? and TNF-? induce neurotoxicity through glutamate production: a potential role for neuronal glutaminase. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.5.1.2 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32483415&form=6&db=m Dendrimer-conjugated glutaminase inhibitor selectively targets microglial glutaminase in a mouse model of Rett syndrome. ongoing research,therapeutic application,unassigned 1,4,0 3.5.1.2 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33957830&form=6&db=m Glutaminase inhibitory activities of pentacyclic triterpenes isolated from Thymus vulgaris L. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26546362&form=6&db=m Glutaminase-containing microvesicles from HIV-1-infected macrophages and immune-activated microglia induce neurotoxicity. causal interaction,unassigned 3,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27339732&form=6&db=m Gut microbiota drive the development of neuroinflammatory response in cirrhosis in mice. diagnostic usage,ongoing research,unassigned 3,2,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28427419&form=6&db=m TNF-? promotes extracellular vesicle release in mouse astrocytes through glutaminase. causal interaction,therapeutic application,unassigned 3,1,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28624534&form=6&db=m Glutaminase C overexpression in the brain induces learning deficits, synaptic dysfunctions, and neuroinflammation in mice. unassigned - 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29540215&form=6&db=m Glutaminase 1 regulates the release of extracellular vesicles during neuroinflammation through key metabolic intermediate alpha-ketoglutarate. unassigned - 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31661467&form=6&db=m ?1-Integrin- and KV1.3 channel-dependent signaling stimulates glutamate release from Th17 cells. therapeutic application,unassigned 3,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32117296&form=6&db=m Glutaminase 1 Regulates Neuroinflammation After Cerebral Ischemia Through Enhancing Microglial Activation and Pro-Inflammatory Exosome Release. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32121257&form=6&db=m Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats. unassigned - 3.5.1.2 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33278560&form=6&db=m Glutaminase in microglia: A novel regulator of neuroinflammation. unassigned - 3.5.1.2 Osteoporosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31112871&form=6&db=m MicroRNA-200a-3p accelerates the progression of osteoporosis by targeting glutaminase to inhibit osteogenic differentiation of bone marrow mesenchymal stem cells. therapeutic application,unassigned 1,0 3.5.1.2 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2865980&form=6&db=m [13N]Ammonia and L-[amide-13N]glutamine metabolism in glutaminase-sensitive and glutaminase-resistant murine tumors. causal interaction,ongoing research,therapeutic application,unassigned 1,2,1,0 3.5.1.2 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30338824&form=6&db=m Significance of neoadjuvant chemotherapy (NACT) in limb salvage treatment of osteosarcoma and its effect on GLS1 expression. ongoing research,therapeutic application,unassigned 2,2,0 3.5.1.2 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31404800&form=6&db=m Acetone immersion enhanced MALDI-MS imaging of small molecule metabolites in biological tissues. ongoing research,unassigned 1,0 3.5.1.2 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32158544&form=6&db=m Glutaminase-1 (GLS1) inhibition limits metastatic progression in osteosarcoma. causal interaction,therapeutic application,unassigned 4,2,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11033463&form=6&db=m Localization of phosphate dependent glutaminase in ascites fluid of ovarian cancer patient. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,1,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11876557&form=6&db=m Effect of purified glutaminase from human ascites fluid on experimental tumor bearing mice. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,4,3 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15743040&form=6&db=m Modulation of tumor induced angiogenesis in Ehrlich ascites tumor. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,4,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18697567&form=6&db=m Acivicin with glutaminase regulates proliferation and invasion of human MCF-7 and OAW-42 cells--an in vitro study. causal interaction,therapeutic application,unassigned 1,3,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27191653&form=6&db=m Altered glutamine metabolism in platinum resistant ovarian cancer. diagnostic usage,therapeutic application,unassigned 3,1,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27784287&form=6&db=m Induction of autophagy by ARHI (DIRAS3) alters fundamental metabolic pathways in ovarian cancer models. ongoing research,unassigned 2,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27830010&form=6&db=m Glutaminase inhibitor compound 968 inhibits cell proliferation and sensitizes paclitaxel in ovarian cancer. diagnostic usage,ongoing research,therapeutic application,unassigned 3,3,2,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29633308&form=6&db=m Molecular targeting of glutaminase sensitizes ovarian cancer cells to chemotherapy. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,3,4 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31449760&form=6&db=m Defining and targeting wild-type BRCA high-grade serous ovarian cancer: DNA repair and cell cycle checkpoints. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32859605&form=6&db=m Inhibition of the MYC-regulated glutaminase metabolic axis is an effective synthetic lethal approach for treating chemoresistant cancers. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27559084&form=6&db=m Combination therapy with BPTES nanoparticles and metformin targets the metabolic heterogeneity of pancreatic cancer. causal interaction,ongoing research,therapeutic application,unassigned 4,1,4,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30563888&form=6&db=m Nutrient stress-dysregulated antisense lncRNA GLS-AS impairs GLS-mediated metabolism and represses pancreatic cancer progression. ongoing research,therapeutic application,unassigned 2,1,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31231915&form=6&db=m Upregulation of the Glutaminase II Pathway Contributes to Glutamate Production upon Glutaminase 1 Inhibition in Pancreatic Cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31911550&form=6&db=m Undermining Glutaminolysis Bolsters Chemotherapy While NRF2 Promotes Chemoresistance in KRAS-Driven Pancreatic Cancers. causal interaction,therapeutic application,unassigned 2,4,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33513833&form=6&db=m TFEB Supports Pancreatic Cancer Growth through the Transcriptional Regulation of Glutaminase. therapeutic application,unassigned 1,0 3.5.1.2 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33672789&form=6&db=m Nrf2 Activation Sensitizes K-Ras Mutant Pancreatic Cancer Cells to Glutaminase Inhibition. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.5.1.2 Pancreatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22684410&form=6&db=m L: -Asparaginase as Potent Anti-leukemic Agent and Its Significance of Having Reduced Glutaminase Side Activity for Better treatment of Acute Lymphoblastic Leukaemia. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Pick Disease of the Brain http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2213015&form=6&db=m Enzyme activities in relation to pH and lactate in postmortem brain in Alzheimer-type and other dementias. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,1,0 3.5.1.2 Polycystic Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29420817&form=6&db=m Glutamine metabolism via glutaminase 1 in autosomal-dominant polycystic kidney disease. causal interaction,unassigned 1,0 3.5.1.2 Polycythemia Vera http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4718814&form=6&db=m [L-asparaginase and L-glutaminase activities in leukocytes and plasma in polycythemia vera] causal interaction,diagnostic usage,ongoing research,unassigned 2,2,1,0 3.5.1.2 Potassium Deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4010646&form=6&db=m Relationship of phosphate-dependent glutaminase activity to ammonia excretion in potassium deficiency and acidosis. unassigned - 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6947966&form=6&db=m L-glutaminase and L-asparaginase by extracorporeal route in acute lymphoblastic leukemia therapy. causal interaction,diagnostic usage,therapeutic application,unassigned 1,1,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9349841&form=6&db=m Low glutamine concentrations induce phenotypical and functional differentiation of U937 myelomonocytic cells. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11106175&form=6&db=m Engineering the substrate specificity of Escherichia coli asparaginase. II. Selective reduction of glutaminase activity by amino acid replacements at position 248. therapeutic application,unassigned 4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22042278&form=6&db=m In silico engineering of L-asparaginase to have reduced glutaminase side activity for effective treatment of acute lymphoblastic leukemia. causal interaction,therapeutic application,unassigned 4,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26413120&form=6&db=m Purification and Characterization of Asparaginase from Phaseolus vulgaris Seeds. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26597158&form=6&db=m Purification and characterization of glutaminase free asparaginase from Pseudomonas otitidis: Induce apoptosis in human leukemia MOLT-4 cells. causal interaction,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26742323&form=6&db=m Isolation and identification of actinomycetes for production of novel extracellular glutaminase free L-asparaginase. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26992786&form=6&db=m Enhanced catalysis of l-asparaginase from Bacillus licheniformis by a rational redesign. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27330530&form=6&db=m The potential of halophilic and halotolerant bacteria for the production of antineoplastic enzymes: L-asparaginase and L-glutaminase. causal interaction,therapeutic application,unassigned 1,4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29447943&form=6&db=m Novel mutant of Escherichia coli asparaginase II to reduction of the glutaminase activity in treatment of acute lymphocytic leukemia by molecular dynamics simulations and QM-MM studies. therapeutic application,unassigned 4,0 3.5.1.2 Precursor Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31209181&form=6&db=m Glutaminase Activity of L-Asparaginase Contributes to Durable Preclinical Activity against Acute Lymphoblastic Leukemia. diagnostic usage,ongoing research,therapeutic application,unassigned 1,3,2,0 3.5.1.2 Precursor T-Cell Lymphoblastic Leukemia-Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31919076&form=6&db=m WEE1 inhibition induces glutamine addiction in T-cell acute lymphoblastic leukemia. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19219026&form=6&db=m c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism. causal interaction,ongoing research,unassigned 1,3,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25482439&form=6&db=m Elevated expression of glutaminase confers glucose utilization via glutaminolysis in prostate cancer. causal interaction,diagnostic usage,unassigned 3,3,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30009389&form=6&db=m NRH:quinone oxidoreductase 2 (NQO2) and glutaminase (GLS) both play a role in large extracellular vesicles (LEV) formation in preclinical LNCaP-C4-2B prostate cancer model of progressive metastasis. ongoing research,unassigned 2,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30103944&form=6&db=m c-Myc-driven glycolysis via TXNIP suppression is dependent on glutaminase-MondoA axis in prostate cancer. therapeutic application,unassigned 1,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33753479&form=6&db=m A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33947068&form=6&db=m Evaluation of Glutaminase Expression in Prostate Adenocarcinoma and Correlation with Clinicopathologic Parameters. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 3.5.1.2 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34486482&form=6&db=m Targeting glutamine metabolism and autophagy: the combination for prostate cancer radiosensitization. unassigned - 3.5.1.2 Psoriasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32831293&form=6&db=m GLS1-mediated glutaminolysis unbridled by MALT1 protease promotes psoriasis pathogenesis. ongoing research,unassigned 2,0 3.5.1.2 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30943369&form=6&db=m Inhibition of Glutaminase 1 Attenuates Experimental Pulmonary Fibrosis. causal interaction,therapeutic application,unassigned 2,4,0 3.5.1.2 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32519817&form=6&db=m SIRT7-mediated modulation of glutaminase 1 regulates TGF-?-induced pulmonary fibrosis. causal interaction,unassigned 3,0 3.5.1.2 Pyelonephritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1233278&form=6&db=m [Renal glutaminase I activities in experimental and human chronic pyelonephritis (author's transl)] ongoing research,unassigned 4,0 3.5.1.2 Renal Insufficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5792214&form=6&db=m Glutaminase activity of the kidney in experimental renal failure of rats. ongoing research,unassigned 4,0 3.5.1.2 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=919372&form=6&db=m [Activity of glutamine deaminating enzymes in the kidneys, liver and serum of dogs with renal failure and under normal conditions] unassigned - 3.5.1.2 Reperfusion Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7809922&form=6&db=m The effects of administration of nitric oxide inhibitors during small bowel preservation and reperfusion. diagnostic usage,ongoing research,unassigned 1,3,0 3.5.1.2 Reperfusion Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34445210&form=6&db=m Mitochondrial Metabolism behind Region-Specific Resistance to Ischemia-Reperfusion Injury in Gerbil Hippocampus. Role of PKC?II and Phosphate-Activated Glutaminase. unassigned - 3.5.1.2 Respiratory Insufficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30575854&form=6&db=m Identification of a Loss-of-Function Mutation in the Context of Glutaminase Deficiency and Neonatal Epileptic Encephalopathy. causal interaction,unassigned 4,0 3.5.1.2 Rett Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32483415&form=6&db=m Dendrimer-conjugated glutaminase inhibitor selectively targets microglial glutaminase in a mouse model of Rett syndrome. ongoing research,therapeutic application,unassigned 1,4,0 3.5.1.2 Sarcoma, Myeloid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6572560&form=6&db=m Prominent glutamine oxidation activity in mitochondria of hematopoietic tumors. diagnostic usage,unassigned 1,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2884278&form=6&db=m Acute and long-term effects of chlorpromazine on glutamine synthetase and glutaminase in rat brain. ongoing research,unassigned 3,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5795584&form=6&db=m [Metabolic studies on epileptic seizures. The activity of glutaminase and glutamine synthetase and ammonia metabolism before and during cerebral convulsions] ongoing research,unassigned 3,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=6145159&form=6&db=m Studies on sound-induced epilepsy in mice. therapeutic application,unassigned 1,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20492947&form=6&db=m Functional significance of the activities of glutaminase and ornithine-?-aminotransferase in rat brain. diagnostic usage,ongoing research,unassigned 1,1,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30575854&form=6&db=m Identification of a Loss-of-Function Mutation in the Context of Glutaminase Deficiency and Neonatal Epileptic Encephalopathy. causal interaction,unassigned 4,0 3.5.1.2 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33657439&form=6&db=m Pentylenetetrazol-induced seizures in adult rats are associated with plastic changes to the dendritic spines on hippocampal CA1 pyramidal neurons. causal interaction,unassigned 2,0 3.5.1.2 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9124626&form=6&db=m Increased glutamine consumption in small intestine epithelial cells during sepsis in rats. causal interaction,unassigned 3,0 3.5.1.2 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10374488&form=6&db=m [Influence of recombinant growth hormone on protein metabolism during severe infection: an animal experiment] diagnostic usage,ongoing research,unassigned 3,1,0 3.5.1.2 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21073932&form=6&db=m Berberine attenuates lipopolysaccharide-induced impairments of intestinal glutamine transport and glutaminase activity in rat. causal interaction,therapeutic application,unassigned 2,1,0 3.5.1.2 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25218789&form=6&db=m Hepatic encephalopathy in patients with acute decompensation of cirrhosis and acute-on-chronic liver failure. causal interaction,unassigned 1,0 3.5.1.2 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33450358&form=6&db=m Glutaminase inhibition with telaglenastat (CB-839) improves treatment response in combination with ionizing radiation in head and neck squamous cell carcinoma models. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1538831&form=6&db=m Effect of starvation or streptozotocin-diabetes on phosphate-activated glutaminase of different rat brain regions. ongoing research,unassigned 4,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1982377&form=6&db=m [Features of the interconversion of alpha-ketoglutarate--glutamate in brain mitochondria of exothermic animals during hibernation] causal interaction,unassigned 3,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4074334&form=6&db=m Fuel utilization in colonocytes of the rat. causal interaction,unassigned 1,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=7126190&form=6&db=m Effects of starvation on the maximal activities of some glycolytic and citric acid-cycle enzymes and glutaminase in mucosa of the small intestine of the rat. ongoing research,unassigned 4,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8145070&form=6&db=m Transcriptional control of rat hepatic glutaminase expression by dietary protein level and starvation. diagnostic usage,ongoing research,unassigned 3,2,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8262331&form=6&db=m Hepatic glutaminase expression: relationship to kidney-type glutaminase and to the urea cycle. unassigned - 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8527215&form=6&db=m Regulation of glutaminase activity and glutamine metabolism. causal interaction,unassigned 1,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9787797&form=6&db=m Distribution of phosphate-activated glutaminase isozymes in the chicken: absence from liver but presence of high activity in pectoralis muscle. unassigned - 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11044634&form=6&db=m Starvation alters the activity and mRNA level of glutaminase and glutamine synthetase in the rat intestine. diagnostic usage,ongoing research,therapeutic application,unassigned 4,4,1,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28750681&form=6&db=m Drug-induced amino acid deprivation as strategy for cancer therapy. therapeutic application,unassigned 3,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30993582&form=6&db=m Isolation and screening of extracellular anticancer enzymes from halophilic and halotolerant bacteria from different saline environments in Iran. diagnostic usage,ongoing research,unassigned 3,1,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31980651&form=6&db=m Targeting glutamine metabolism slows soft tissue sarcoma growth. causal interaction,diagnostic usage,unassigned 2,2,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33087507&form=6&db=m Glutaminase Inhibitors Induce Thiol-Mediated Oxidative Stress and Radiosensitization in Treatment-Resistant Cervical Cancers. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,3,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33762340&form=6&db=m LncRNA GIRGL drives CAPRIN1-mediated phase separation to suppress glutaminase-1 translation under glutamine deprivation. unassigned - 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33895866&form=6&db=m Glutamine deficiency promotes stemness and chemoresistance in tumor cells through DRP1-induced mitochondrial fragmentation. causal interaction,ongoing research,therapeutic application,unassigned 1,1,4,0 3.5.1.2 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33911160&form=6&db=m Inhibition of eEF2K synergizes with glutaminase inhibitors or 4EBP1 depletion to suppress growth of triple-negative breast cancer cells. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=990468&form=6&db=m [Concentration of free glutamine and glutaminase activity in the gastric mucosa of patients with precancerous diseases and cancer of the stomach] diagnostic usage,ongoing research,unassigned 1,4,0 3.5.1.2 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29032577&form=6&db=m Pyruvate kinase isozyme M2 and glutaminase might be promising molecular targets for the treatment of gastric cancer. therapeutic application,unassigned 4,0 3.5.1.2 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30485682&form=6&db=m iTRAQ-Based Quantitative Proteomics Approach Identifies Novel Diagnostic Biomarkers That Were Essential for Glutamine Metabolism and Redox Homeostasis for Gastric Cancer. diagnostic usage,ongoing research,therapeutic application,unassigned 3,3,1,0 3.5.1.2 Thrombosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22684410&form=6&db=m L: -Asparaginase as Potent Anti-leukemic Agent and Its Significance of Having Reduced Glutaminase Side Activity for Better treatment of Acute Lymphoblastic Leukaemia. causal interaction,therapeutic application,unassigned 4,1,0 3.5.1.2 Thyroid Cancer, Papillary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29942976&form=6&db=m Targeting glutaminase-mediated glutamine dependence in papillary thyroid cancer. causal interaction,ongoing research,unassigned 2,4,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24523301&form=6&db=m Antitumor Activity of the Glutaminase Inhibitor CB-839 in Triple-Negative Breast Cancer. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,4,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28185053&form=6&db=m Glutaminase expression is a poor prognostic factor in node-positive triple-negative breast cancer patients with a high level of tumor-infiltrating lymphocytes. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28950000&form=6&db=m Glutaminase is essential for the growth of triple-negative breast cancer cells with a deregulated glutamine metabolism pathway and its suppression synergizes with mTOR inhibition. causal interaction,unassigned 4,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30072394&form=6&db=m Glutamate-Weighted Chemical Exchange Saturation Transfer Magnetic Resonance Imaging Detects Glutaminase Inhibition in a Mouse Model of Triple-Negative Breast Cancer. therapeutic application,unassigned 3,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31040181&form=6&db=m Dual inhibition of glutaminase and carnitine palmitoyltransferase decreases growth and migration of glutaminase inhibition-resistant triple-negative breast cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,3,3 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33176943&form=6&db=m Discovery and optimization of withangulatin A derivatives as novel glutaminase 1 inhibitors for the treatment of triple-negative breast cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33911160&form=6&db=m Inhibition of eEF2K synergizes with glutaminase inhibitors or 4EBP1 depletion to suppress growth of triple-negative breast cancer cells. causal interaction,therapeutic application,unassigned 3,4,0 3.5.1.2 Tuberculosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5486084&form=6&db=m [Glutaminase activity and intensity of glutamine metabolism in the lungs and lymph nodes in tuberculosis] diagnostic usage,unassigned 3,0 3.5.1.2 Tuberculosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19270703&form=6&db=m Regulation of active site coupling in glutamine-dependent NAD(+) synthetase. diagnostic usage,ongoing research,therapeutic application,unassigned 3,3,1,0 3.5.1.2 Tuberculosis, Pulmonary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=4767521&form=6&db=m [Activity of blood glutaminase in patients with pulmonary tuberculosis and other diseases] causal interaction,diagnostic usage,unassigned 1,4,0 3.5.1.2 Uremia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=5822023&form=6&db=m [Amylase metabolism and changes in glutaminase and glutamate-synthetase activity in brain during experimental uremia] ongoing research,unassigned 2,0 3.5.1.2 Urinary Bladder Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30458442&form=6&db=m miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.5.1.2 Urinary Bladder Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30902882&form=6&db=m LincRNA-p21 suppresses glutamine catabolism and bladder cancer cell growth through inhibiting glutaminase expression. therapeutic application,unassigned 1,0 3.5.1.2 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23954443&form=6&db=m Knock-down of glutaminase 2 expression decreases glutathione, NADH, and sensitizes cervical cancer to ionizing radiation. ongoing research,unassigned 3,0 3.5.1.2 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33087507&form=6&db=m Glutaminase Inhibitors Induce Thiol-Mediated Oxidative Stress and Radiosensitization in Treatment-Resistant Cervical Cancers. diagnostic usage,ongoing research,therapeutic application,unassigned 3,2,3,0 3.5.1.2 Vitamin E Deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14274653&form=6&db=m [GLUTAMINASE ACTIVITY OF THE SKELETAL MUSCLE CELLS UNDER NORMAL CONDITIONS AND IN VITAMIN E DEFICIENCY.] ongoing research,unassigned 4,0 3.5.1.2 Xeroderma Pigmentosum http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9828143&form=6&db=m Physical and genetic linkage of glutaminase (Gls), signal transducer and activator of transcription 1 (Stat1), and xeroderma pigmentosum complementation group G (Xpg) on mouse proximal chromosome 1. ongoing research,unassigned 1,0