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2.7.1.91: sphingosine kinase

This is an abbreviated version!
For detailed information about sphingosine kinase, go to the full flat file.

Word Map on EC 2.7.1.91

Reaction

ATP
+
a sphingoid base
=
ADP
 +
a sphingoid base 1-phosphate

Synonyms

dihydrosphingosine kinase, kinase, dihydrosphingosine (phosphorylating), kinase, sphingosine (phosphorylating), More, SGK, SK, SK-1, SK-2, SK1, SK2, sphinganine kinase, sphingoid base kinase, sphingosine kinase, sphingosine kinase 1, sphingosine kinase 2, sphingosine kinase type 1, sphingosine kinase type 2, sphingosine kinase-1, sphingosine kinase-2, SPHK, SPHK-1, SPHK1, SPHK1a, SPHK1b, SPHK2, SPK

ECTree

     2 Transferases
         2.7 Transferring phosphorus-containing groups
             2.7.1 Phosphotransferases with an alcohol group as acceptor
                2.7.1.91 sphingosine kinase

Expression

Expression on EC 2.7.1.91 - sphingosine kinase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
both lipopolysaccharide and thrombin increase mouse lung microvascular permeability and result in a delayed activation of SPHK1 that is coupled to the onset of restoration of pulmonary microvessel permeability
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dihydrotestosterone triggers cell growth in steroid-deprived MC-3T3 cells, associated with a rapid stimulation of isoform SphK1 and activation of both Akt and ERK signaling pathways. This mechanism relies on functional androgen receptor/PI3K/Akt nongenotropic signaling as pharmacological antagonists can block SphK1 stimulation by dihydrotestosterone and its consequences. SphK1 inhibition also blocks cell proliferation, while ERK inhibition has no impact
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enzyme expression is increased in microglia subjected to oxygen-glucose deprivation
hypoxia increases SK1 mRNA levels, protein expression, and enzyme activity, followed by intracellular sphingosine 1-phosphate production and sphingosine 1-phosphate release. Knockdown of hypoxia-inducible factor HIF-2 by small interfering RNA abolishes the induction of SK1 and the production of extracellular shpingosine 1-phosphate after CoCl2 treatment, whereas HIF-1 small interfering RNA results in an increase of HIF-2 and of SK1 protein levels. HIF-2 binds the SK1 promoter
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in bronchial epithelial cells, SphK1 and MUC5AC expression is increased by IL-13 treatment at both protein and mRNA levels, whereas SphK2 expression is not changed. Inhibitor N,N-dimethylsphingosine decreases MUC5AC expression up-regulated by IL-13 treatment and inhibits IL-13-induced ERK1/2 phosphorylation but neither p38 MAPK nor STAT6 phosphorylation
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inhibition of protein kinase C-alpha, signal transducers and activators of transcription 3 and c-Jun NH2-terminal kinase inhibition suppresses SPHK1 expression in v-Src-transformed NIH-3T3 cells, whereas their overexpression increases SPHK1 mRNA. Modulation of AUF1 and HuR by their overexpression or siRNA reveals that SPHK1 mRNA in v-Src- and mock-NIH3T3 is regulated reciprocally by these factors
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isoform SPHK1 expression is significantly elevated after exposure to hydrogen peroxide
knockdown of isoform SK2 expression results in overexpression of isoform SK1 in several cell lines. Treatment with inhibitor (2S,3R,4E)-2-(dimethylamino)octadec-4-ene-1,3-diol triples the levels of isoform SK1 mRNA, but only slightly increases isoform SK2 expression. Treatment with inhibitor 2-(4-hydroxyanilino)-4-(4-chlorophenyl)thiazole increases mRNAs for both isoforms SK1 and SK2 by about 4fold
long-term removal of androgen support in LNCaP and C4-2B cells results in a progressive increase in SphK1 expression and activity throughout the progression to androgen-independence state, which is characterized by the acquisition of a neuroendocrine-like cell phenotype
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sphingosine kinase-1 transcript levels are higher in human primary melanomas as compared to nevi
SphK1 inhibition by docetaxel is a two-step process involving an initial loss of enzyme activity followed by a decrease in SphK1 gene expression. Both pharmacological and siRNA-mediated SphK1 inhibition leads to a four-fold decrease in the docetaxel IC50 dose
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the expression of IL-1 correlates with the expression of SphK1 in glioblastoma cells. IL-1 up-regulates SphK1 mRNA levels, protein expression, and activity in both primary human astrocytes and various glioblastoma cell lines, it does not affect SphK2 expression. The IL-1-induced SphK1 up-regulation can be blocked by the inhibition of c-Jun N-terminal kinase, the overexpression of the dominant-negative c-Jun(TAM67), and the down-regulation of c-Jun expression by small interference RNA. Activation of SphK1 expression by IL-1 occurs on the level of transcription and is mediated via a novel AP-1 element located within the first intron of the sphk1 gene
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transforming growth factor TGF-beta2 activates the promoter of isoform Sk1, resulting in upregulation of its mRNa and protein expression
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treatment with inhibitors N,N-dimethylsphingosine or DL-threo-dihydrosphingosine or with doxorubicin leads to increase in expression as a result of apoptotic stress. The caspase inhibitor ZVAD reduces not only doxorubicin-induced lethality but also the increased expression of SphK1 and secretion of sphingosine 1-phosphate
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treatment with lipopolysaccharid causes significantly enhances isoform SphK1 expression within 6 h, which declines back to baseline levels by 24 h. Expression of isoform SphK2 is gradually induced following lipopolysaccharide treatment and is elevated within 24 h
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treatment with lipopolysaccharide increases the SphK1 mRNA and protein expression in microglia leading to altered expression and production of proinflammatory cytokines and nitric oxide. Suppression of SphK1 by its inhibitor, N, N-dimethylsphingosine, or siRNA results in decreased mRNA expression of TNF-alpha, IL-1beta and iNOS and release of TNF-alpha and nitric oxide in lipopolysaccharid-activated microglia
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v-Src-transfected cells show both increased SPHK1 mRNA and enzyme activity. Inhibition of protein kinase C-alpha, signal transducers and activators of transcription 3 and c-Jun NH2-terminal kinase inhibition suppresses SPHK1 expression in v-Src-transformed NIH-3T3 cells, whereas their overexpression increases SPHK1 mRNA. Modulation of AUF1 and HuR by their overexpression or siRNA reveals that SPHK1 mRNA in v-Src- and mock-NIH3T3 is regulated reciprocally by these factors
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