EC Number   |
General Information |
Reference |
|---|
   2.7.1.138 | malfunction |
a mutation in ceramide kinase specifically leads to proteolysis of NORPA, consequent loss of phosphoinositide-specific phospholipase C activity, and failure in light signal transduction, a significant increase in ceramide, resulting from lack of ceramide kinase, perturbs the membrane microenvironment of phosphatidylinositol-4,5-bisphosphate, altering its distribution |
701002 |
| 2.7.1.138 | malfunction |
a specific inhibitor of ceramide kinase inhibits TGF-beta-induced migration of BM-MSCs and N-cadherin that is necessary for BM-MSCs migration in response to TGF-beta |
760496 |
| 2.7.1.138 | malfunction |
Arabidopsis thaliana cell-death mutant, accelerated cell death5 (acd5), which accumulates ceramides and exhibits spontaneous cell death late in development. NaCl enhances disease resistance and suppresses cell death in ceramide kinase mutants partly via a mechanism that depends on abscisic acid (ABA) and salicylic acid (SA) antagonistic interaction, and enhances disease resistance independent of pattern-triggered immune responses. 300 mM NaCl suppresses the cell-death phenotype of the acd5 mutant without inhibiting plant growth |
762163 |
| 2.7.1.138 | malfunction |
capillary-like tube formation is significantly impaired in CerK-deficient cells or in wild type cells treated with NVP-231 as compared with untreated wild type cells, ceramide kinase ablation increases serum ceramide levels at the expense of dihydroceramide levels without affecting sphingosine, dihydrosphingosine, sphingosine-1-phosphate or dihydrosphingosine-1-phosphate levels, in both Cerk -/- and NVP-231-treated cells, the density of the cell monolayer area is in increased at the expense of the tube forming area |
700070 |
| 2.7.1.138 | malfunction |
cells lacking acid sphingomyelinase (ASM) have decreased ceramide 1-phosphate production following TNF-alpha treatment, suggesting that ASM may be acting upstream of CERK. Effect of CERK knockdown on lipid levels of ceramide 1-phosphate, ceramide, and sphingosine, overview. Knockdown of CERK in the presence of ASM overexpression led to a decrease in CCL5 levels on the protein and message levels |
761664 |
| 2.7.1.138 | malfunction |
genetic ablation of CERK reduces basal ceramide 1-phosphate levels. CERK-/- knockout mouse cells show 52-74% reduced ceramide 1-phosphate contents and significantly lower levels of multiple eicosanoids compared to wild-type. Induction of eicosanoid synthesis by calcium ionophore is significantly reduced in the CERK-/- primary mouse embryonic fibroblasts. The CERK-/- mouse has adapted to loss of CERK in regards to airway hyper-responsiveness as compared with CERK siRNA treatment. Eicosanoids produced by immortalized primary mouse embryonic fibroblasts, overview |
-, 738824 |
| 2.7.1.138 | malfunction |
genetic ablation of CERK results in decreased levels of ceramide 1-phosphate in fibroblasts and inhibits the ability of fibroblasts to release arachidonic acid in response to mechanical trauma. Simulation of mechanical trauma of a wound by scratching a monolayer of fibroblasts from CERK+/+ mice demonstrates steadily increasing levels of arachidonic acid in a time-dependent manner in stark contrast to CERK-/- fibroblasts, reflected in scratch-induced eicosanoid levels. Loss of proper eicosanoid response translated into an abnormal migration pattern for the fibroblasts isolated from CERK-/-. Neither the wild-type nor the CERK-null fibroblasts demonstrated additional changes to the endogenous ceramide 1-phosphate content upon induction of mechanical trauma. The migratory response to wounding of CERK-/- fibroblasts can be rescued via the addition of exogenous eicosanoids |
-, 738825 |
| 2.7.1.138 | malfunction |
knockdown of CerK and overexpression of HA-tagged CerK down- and upregulated the formation of ceramide-1-phosphate (C1P), respectively. When knockdown or overexpression of CerK is performed, Ca2+-induced release of [3H] noradrenaline is reduced or enhanced, respectively, but neurite extension is not modified. A limited change in cellular sphingolipid levels by knockdown of CerK. The levels of ceramide, sphingomyelin, and monohexosylceramide, including their total levels and levels of their subspecies with irrespective of N-acyl chain lengths, and those of sphingosine, sphingomyelin 1-phosphate, and their dihydro-forms are not affected by the CerK knockdown in PC12 cells |
760632 |
| 2.7.1.138 | malfunction |
loss of CerK sensitized cells towards stress-induced apoptosis, loss of CerK facilitates apoptosis induced by stress factors such as staurosporine or TNFalpha combined with cycloheximide. Cell treatment with enzyme inhibitor NVP-231 decreases DNA synthesis, but not agonist-stimulated arachidonic acid release or PGE2 synthesis, overview |
738014 |
| 2.7.1.138 | malfunction |
loss of CerK sensitized cells towards stress-induced apoptosis, loss of CerK facilitates apoptosis induced by stress factors such as staurosporine or TNFalpha combined with cycloheximide. Cell treatment with enzyme inhibitor NVP-231 decreases DNA synthesis, but not agonist-stimulated arachidonic acid release or PGE2 synthesis. Proliferation but not arachidonic acid release or PGE2 synthesis is reduced in CERK knockout cells, overview |
738014 |
