EC Number   |
General Information |
Reference |
|---|
   2.7.3.2 | evolution |
the MtCK gene is likely basal and ancestral and has evolved very early in metazoan evolution |
738079 |
| 2.7.3.2 | malfunction |
24 h after trauma brain injury (TBI) of mice preconditioned with N-methyl-D-aspartate, creatine kinase activity is augmented in the cerebral cortex. Eventhough N-methyl-D-aspartate preconditioning and TBI have similar effects on the enzyme activity, each manages its response via opposite mechanisms because the protective effects of preconditioning are unambiguous |
-, 739050 |
| 2.7.3.2 | malfunction |
absence of creatine kinase in muscle cells leads to morphological and functional adaptations towards preservation of muscle contractile abilities |
703836 |
| 2.7.3.2 | malfunction |
complete brain-type creatine kinase deficiency in mice blocks seizure activity and affects intracellular calcium kinetics |
703504 |
| 2.7.3.2 | malfunction |
downregulation of brain-type creatine kinase in brain of a Huntington's disease mouse model. Huntington's disease is a hereditary neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Mutant HTT (mHTT) suppresses the activity of the CKB gene promoter, which contributes to the lowered CKB expression in Huntington's disease. Exogenous expression of wild-type CKB, but not a dominant negative CKB mutant, rescues the ATP depletion, aggregate formation, impaired proteasome activity, and shortened neurites induced by mHTT. Negative regulation of isozyme CKB by mHTT is a key event in the pathogenesis of Huntington's disease and contributes to the neuronal dysfunction associated with Huntington's disease |
-, 737741 |
| 2.7.3.2 | malfunction |
downregulation of brain-type creatine kinase in brains of Huntington's disease patients. Huntington's disease is a hereditary neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene |
737741 |
| 2.7.3.2 | malfunction |
impairment of enzyme activity leads to a downregulation of renal Na+, K+-ATPase activity during an Aeromonas caviae infection, contributing to energy depletion |
761841 |
| 2.7.3.2 | malfunction |
knockout mice that lack the brain CK isoforms, i.e. BCK and/or ubiquitous MtCK, uMtCK, show defects in spatial memory acquisition and behavior, development of the hippocampus, correct functioning of hair bundle cells in the auditory system, and energy distribution within photoreceptor cells, transgenic models of creatine deficiency, overview |
737427 |
| 2.7.3.2 | malfunction |
oxygen consumption dynamics during electrical stimulation in superfused fast-twitch hindlimb muscles isolated from wild-type and transgenic mice deficient in the myoplasmic and mitochondrial creatine isoforms (MiM CK-/-), respectively. Transgenic mice deficient in the mitochondrial creatinine isoforms (MiM CK-/-) show muscle oxygen consumption activation kinetics 30% faster than wild-type. MiM CK-/- muscle oxygen consumption deactivation kinetics are 380% faster than wild-type |
721259 |
| 2.7.3.2 | metabolism |
co-localization and functional coupling of creatine kinase isoforms with ATP-producing and ATP-consuming reactions, a non-equilibrium state of the creatine kinase reaction, and restricted intracellular diffusion of adenine nucleotides support the concept of a cellular CK/PCr phosphoryl transfer network. spatial organization of the CK/PCr shuttle in brain, in particular the association of BCK to subcellular components as well as to specific, interacting proteins, overview |
-, 737427 |
