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alpha-OH-C24:0 phytoceramide + ATP
alpha-OH-C24:0 phytoceramide 1-phosphate + ADP
-
-
-
-
?
alpha-OH-D-erythro-C6:0 ceramide + ATP
alpha-OH-D-erythro-C6:0 ceramide 1-phosphate + ADP
-
-
-
-
?
ATP + 3-O-methyl C16:0 ceramide
ADP + 3-O-methyl C16:0 ceramide 1-phosphate
-
very low activity
-
-
?
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
ATP + C18-ceramide
ADP + C18-ceramide 1-phosphate
-
lower activity
-
-
?
ATP + C2-ceramide
ADP + C2-ceramide 1-phosphate
-
-
-
-
?
ATP + C8-ceramide
ADP + C8-ceramide 1-phosphate
-
best substrate
-
-
?
ATP + C8-dihydroceramide
ADP + C8-dihydroceramide 1-phosphate
-
high activity
-
-
?
ATP + C8-phytoceramide
ADP + C8-phytoceramide 1-phosphate
-
high activity
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
ATP + D-erythro-C6:0 ceramide
ADP + D-erythro-C6:0 ceramide 1-phosphate
-
very low activity
-
-
?
ATP + D-erythro-N-hexanoyl-sphinganine
ADP + D-erythro-N-hexanoyl-sphinganine 1-phosphate
-
-
-
?
ATP + D-erythro-N-hexanoyl-sphingenine
ADP + D-erythro-N-hexanoyl-sphingenine 1-phosphate
-
-
-
?
ATP + D-eythro-C10:0 ceramide
ADP + D-eythro-C10:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C12:0 ceramide
ADP + D-eythro-C12:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C14:0 ceramide
ADP + D-eythro-C14:0 ceramide 1-phosphate
-
best substrate
-
-
?
ATP + D-eythro-C16:0 (R)-alpha-hydroxyceramide
ADP + D-eythro-C16:0 (R)-alpha-hydroxyceramide 1-phosphate
-
low activity
-
-
?
ATP + D-eythro-C16:0 (S)-alpha-hydroxyceramide
ADP + D-eythro-C16:0 (S)-alpha-hydroxyceramide 1-phosphate
-
very low activity
-
-
?
ATP + D-eythro-C16:0 ceramide
ADP + D-eythro-C16:0 ceramide 1-phosphate
ATP + D-eythro-C16:0 dehydroceramide
ADP + D-eythro-C16:0 dehydroceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C16:0 dihydroceramide
ADP + D-eythro-C16:0 dihydroceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C16:0 urea ceramide
ADP + D-eythro-C16:0 urea ceramide 1-phosphate
-
low activity, no activity with L-e-C16:0 urea ceramide
-
-
?
ATP + D-eythro-C16:0-cis ceramide
ADP + D-eythro-C16:0-cis ceramide 1-phosphate
-
low activity
-
-
?
ATP + D-eythro-C18:0 ceramide
ADP + D-eythro-C18:0 ceramide 1-phosphate
ATP + D-eythro-C18:0 phytoceramide
ADP + D-eythro-C18:0 phytoceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C20:0 ceramide
ADP + D-eythro-C20:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C24:0 ceramide
ADP + D-eythro-C24:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C24:1 ceramide
ADP + D-eythro-C24:1 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C8:0 ceramide
ADP + D-eythro-C8:0 ceramide 1-phosphate
-
low activity
-
-
?
ATP + diacylglycerol
ADP + diacylglycerol 1-phosphate
-
-
-
-
?
ATP + hexadecanoylceramide
ADP + hexadecanoylceramide 1-phosphate
C8 acyl chain, slightly higher activity than with natural ceramide
-
?
ATP + hexanoylceramide
ADP + hexanoylceramide 1-phosphate
C6 acyl chain, similar activity than with natural ceramide, very low activity with C2-ceramide and C6-dihydroceramide, no activity with C2-dihydroceramide
-
?
ATP + N-acetyl-D-erythro-sphingenine
ADP + N-acetyl-D-erythro-sphingenine 1-phosphate
-
-
-
?
ATP + N-acetyl-sphingenine
ADP + N-acetyl-sphingenine 1-phosphate
-
-
-
?
ATP + N-hexadecanoyl-sphingenine
ADP + N-hexadecanoyl-sphingenine 1-phosphate
ATP + N-hexanoyl-1-O-hexadecyl-2-deoxy-2-amino-sn-glycerol
ADP + ?
-
-
-
?
ATP + N-hexanoyl-D-erythro-sphingenine
ADP + N-hexanoyl-D-erythro-sphingenine 1-phosphate
best substrate
-
-
?
ATP + N-hexanoyl-sphingenine
ADP + N-hexanoyl-sphingenine 1-phosphate
-
-
-
?
ATP + N-tetradecanoyl-(2S)-amino-butan-1-ol
ADP + ?
-
-
-
?
ATP + N-tetradecanoyl-(2S)-amino-hexadecan-1-ol
ADP + ?
-
-
-
?
ATP + N-tetradecanoyl-2-amino-1-butanol
ADP + ?
-
-
-
?
ATP + N-tetradecanoyl-2S-amino-1-butanol
ADP + ?
-
-
-
?
ATP + octanoylceramide
ADP + octanoylceramide 1-phosphate
C8 acyl chain, higher activity than with natural ceramide
-
?
ATP + octanoyldihydroceramide
ADP + octanoyldihydroceramide 1-phosphate
C8 acyl chain, slightly higher activity than with natural ceramide
-
?
ATP + stearoylceramide
ADP + stearoylceramide 1-phosphate
-
-
-
?
C12-ceramide + ATP
C12-ceramide 1-phosphate + ADP
-
-
-
-
?
C16-ceramide + ATP
C16-ceramide 1-phosphate + ADP
-
-
-
?
C2-ceramide + ATP
C2-ceramide 1-phosphate + ADP
C26:0 phytoceramide + ATP
C26:0 phytoceramide 1-phosphate + ADP
-
-
-
-
?
C8-ceramide + ATP
C8-ceramide 1-phosphate + ADP
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
D-erythro-C12:0 ceramide + ATP
D-erythro-C12:0 ceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-C14:0 ceramide + ATP
D-erythro-C14:0 ceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-C16:0 ceramide + ATP
D-erythro-C16:0 ceramide 1-phosphate + ADP
-
used for kinetic analysis of ceramide kinase activity
-
-
?
D-erythro-C2:0 ceramide + ATP
D-erythro-C2:0 ceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-C2:0 dihydroceramide + ATP
D-erythro-C2:0 dihydroceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-C6:0 ceramide + ATP
D-erythro-C6:0 ceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-C6:0 dihydroceramide + ATP
D-erythro-C6:0 dihydroceramide 1-phosphate + ADP
-
-
-
-
?
D-erythro-N-hexanoyl-sphingenine + ATP
D-erythro-N-hexanoyl-sphingenine 1-phosphate + ADP
-
D-erythro isomer of C6-ceramide, the specific CERK activity in cells exposed for 16-18 h to 0.005 mM C6-ceramide dropped to 18.7%
-
-
?
D-threo-C6-ceramide + ATP
D-threo-C6-ceramide 1-phosphate + ADP
-
no or only weakly decrease of the specific CERK activity
-
-
?
GTP + ceramide
GDP + ceramide 1-phosphate
-
26% of the activity with ATP at 1 mM
-
?
L-erythro-C6-ceramide + ATP
L-erythro-C6-ceramide 1-phosphate + ADP
-
no or only weakly decrease of the specific CERK activity
-
-
?
L-threo-C6-ceramide + ATP
L-threo-C6-ceramide 1-phosphate + ADP
-
no or only weakly decrease of the specific CERK activity
-
-
?
N-((4-(4,4-difluoro-5-(2-thienyl)-4-bora-3alpha,4alpha-diaza-s-indacene-3-yl)phenoxy)acetyl)sphingosine + ATP
N-((4-(4,4-difluoro-5- (2-thienyl)-4- bora-3a,4a-diaza-s-indacene-3-yl)phenoxy)acetyl)sphingosine 1-phosphate + ADP
-
TRB-ceramide
-
-
?
N-(12-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)dodecanoyl)-D-erythro-sphingosine + ATP
N-(12-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)dodecanoyl)-D-erythro-sphingosine 1-phosphate + ADP
-
C12-NBD ceramide
-
-
?
N-(5-(5,7-dimethyl-BODIPY)-L-pentanoyl)-D-erythrosphingosine + ATP
N-(5-(5,7-dimethyl-BODIPY)-L-pentanoyl)-D-erythrosphingosine 1-phosphate + ADP
-
DMB-C5 ceramide
-
-
?
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine + ATP
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine 1-phosphate + ADP
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythro-sphingosine + ATP
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythro-sphingosine 1-phosphate + ADP
NBD-ceramide
NBD-ceramide 1-phosphate
-
?
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine + ATP
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine 1-phosphate + ADP
N-(8-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)octanoyl)-D-erythro-sphingosine + ATP
N-(8-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)octanoyl)-D-erythro-sphingosine 1-phosphate + ADP
C8-ceramide
-
-
?
N-hexanoyl-sphinganine + ATP
N-hexanoyl-sphinganine 1-phosphate + ADP
-
C6-dihydroceramide
-
-
?
N-octyl-sphingenine + ATP
N-octyl-sphingenine 1-phosphate + ADP
-
C8-ceramine, no or only weakly decrease of the specific CERK activity
-
-
?
additional information
?
-
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
-
-
-
?
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
-
lower activity
-
-
?
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
ceramide is an important regulator of photoreceptor viability
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
ceramide 1-phosphate is a lipid signalling molecule involved in regulation of many physiological processes related to cell proliferation, apoptosis, and inflammation, most of them in concert with sphingosine 1-phosphate, ceramide 1-phosphate might act via extracellular cell surface receptors or intracellularly as second messenger
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
synthesis of the sphingolipid signaling molecule
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
no activity sphingosine, D,L-threo-dihydrosphingosine, N,N-dimethylsphingosine and phyto-sphingosine
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
no activity with 1,2-diacylglycerol
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
in vitro substrate delivery of short chain ceramides requires bovine serum albumin, and a mixed micellar form consisting of octylglucoside and cardiolipin for long chain ceramides, choice of delivery system is important for in vitro activity
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
stereospecific ceramide substrate recognition, the C4-5 trans double bond is important for substrate recognition, a minimum of 12C-acyl chain is required for activity
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
the enzyme is specific for the cramide backbone, acylation of amino group in position 2 is required
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
the pleckstrin homology domain is essential for activity, binding of liposomes
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
other name n-acyl-sphingosine, no activity with CTP, CDPcholine and UDPglucose
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
ceramide phosphorylation may be associated with neurotransmitter release
-
?
ATP + D-eythro-C16:0 ceramide
ADP + D-eythro-C16:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C16:0 ceramide
ADP + D-eythro-C16:0 ceramide 1-phosphate
-
high activity
-
-
?
ATP + D-eythro-C18:0 ceramide
ADP + D-eythro-C18:0 ceramide 1-phosphate
-
-
-
-
?
ATP + D-eythro-C18:0 ceramide
ADP + D-eythro-C18:0 ceramide 1-phosphate
-
high activity
-
-
?
ATP + N-hexadecanoyl-sphingenine
ADP + N-hexadecanoyl-sphingenine 1-phosphate
-
-
-
?
ATP + N-hexadecanoyl-sphingenine
ADP + N-hexadecanoyl-sphingenine 1-phosphate
very low activity
-
-
?
C2-ceramide + ATP
C2-ceramide 1-phosphate + ADP
-
-
-
?
C2-ceramide + ATP
C2-ceramide 1-phosphate + ADP
C2-Cer is a potent inducer of cell death in CerK-expressing cells
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CERK and its product Cer-1-P are implicated in signaling processes, Cer-1-P stimulates DNA synthesis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
673703, 675274, 690404, 690671, 691938, 691965, 692594, 693522, 694006, 694266, 671789 -
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide is a key mediator of cellular apoptosis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is a critical mediator of eicosanoid synthesis, and its product, ceramide 1-phosphate, is required for the production of prostaglandins in response to several inflammatory agonists, CERK requires ceramide actively transported to the trans-Golgi network via ceramide transport protein CERT
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is important for cellular proliferation and survival, activation of cytosolic phospholipase A2, mast cell degranulation, and phagocytosis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CERK and C1P are playing significant biological roles in cell-signaling cascades
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK has important roles in leukocyte functions, including the role in degranulation of mast cells and the phagocytosis of polymorphonuclear leukocytes
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
CERK plays a role in cell signalling
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
increased ceramide 1-phosphate during phagocytosis enhances phagocytosis and phagolysosome formation in COS-1 cells expressing hCERK
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
involvement in inflammatory processes and cell growth
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
key enzyme for controlling ceramide levels
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide 1-phosphate is a sphingolipid that participates in cell signaling, but ceramide kinase is not the only source of ceramide 1-phosphate
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is not the only source of ceramide 1-phosphate, ceramide kinase is important for neutrophil homeostasis, ceramide kinase is important for the defense against Streptococcus pneumoniae infections
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK and C1P are involved in many cell functions, including membrane fusion, phagocytosis and degranulation in mast cells
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK is not necessary for survival but might participate in neuronal functions involving emotional behavior
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK is involved in the regulation of mast cells
-
-
?
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine + ATP
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine 1-phosphate + ADP
C6-ceramide
-
-
?
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine + ATP
N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)amino)hexanoyl)-D-erythro-sphingosine 1-phosphate + ADP
-
C6-NBD ceramide
-
-
?
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine + ATP
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine 1-phosphate + ADP
-
-
-
-
?
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine + ATP
N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl-D-erythrosphingosine 1-phosphate + ADP
-
NBD-Cer, NBD-C6 ceramide
-
-
?
additional information
?
-
-
the enzyme does not play a role in neutrophil priming, the enzyme regulates the activity and translocalization of cytosolic phospholipase isozyme A2alpha, overview, the enzyme is involved in prostaglandin biosynthesis, i.e. intracellular arachidonic acid production, which is blocked by enzyme gene silencing
-
-
?
additional information
?
-
-
the enzyme is a critical mediator of eicosanoid synthesis
-
-
?
additional information
?
-
-
no activity with GTP, no activity with sphingosine and sphinganine, and with diacylglycerol
-
-
?
additional information
?
-
-
substrate specificity and stereochemistry, overview, methylation of the primary hydroxyl group results in loss of activity, the enzyme can use both ceramides with long saturated and long unsaturated fatty acyl chains
-
-
?
additional information
?
-
substrate specificity, stereochemistry
-
-
?
additional information
?
-
-
substrate specificity, stereochemistry
-
-
?
additional information
?
-
2-amino-1-hexadecanol, 1-O-hexadecyl-2-deoxy-2-amino-sn-glycerol, N-tetradecanoyl-2(R)-pyrrolidine-methanol, N-tetradecanoyl-(R)-serine, N-tetradecanoyl-3-hydroxypyrrolidin, N-tetradecanoyl-4-amino-1-butanol, N-tetradecanoyl-3-amino-1-propanol, N-tetradecanoyl-(S)-serine, N-tetradecanoyl-2-benzylserine, N-tetradecanoyl3-phenylserine, N-tetradecanoyl-3-amino-tyrosine, N-tetradecanoyl-1-amino-2-naphthol-4-sulfonic acid, N-tetradecanoyl-3-hydroxy-anthranilic acid, N-tetradecanoyl-4-aminophenol, N-tetradecanoyl-diethanolamine, N-tetradecanoyl-ethanolamine, and N-tetradecanoyl-(S)-phenylalaninol are no substrates
-
-
?
additional information
?
-
-
2-amino-1-hexadecanol, 1-O-hexadecyl-2-deoxy-2-amino-sn-glycerol, N-tetradecanoyl-2(R)-pyrrolidine-methanol, N-tetradecanoyl-(R)-serine, N-tetradecanoyl-3-hydroxypyrrolidin, N-tetradecanoyl-4-amino-1-butanol, N-tetradecanoyl-3-amino-1-propanol, N-tetradecanoyl-(S)-serine, N-tetradecanoyl-2-benzylserine, N-tetradecanoyl3-phenylserine, N-tetradecanoyl-3-amino-tyrosine, N-tetradecanoyl-1-amino-2-naphthol-4-sulfonic acid, N-tetradecanoyl-3-hydroxy-anthranilic acid, N-tetradecanoyl-4-aminophenol, N-tetradecanoyl-diethanolamine, N-tetradecanoyl-ethanolamine, and N-tetradecanoyl-(S)-phenylalaninol are no substrates
-
-
?
additional information
?
-
-
does not bind to lysophosphatidic acid, lysophosphocholine, sphingosine 1-phosphate, phosphatidylethanolamine, phosphatidylcholine, phosphatidic acid, or phosphatidylserine
-
-
?
additional information
?
-
activity of CerK in cells is measured by the formation of NBD-C1P from a substrate NBD-ceramide
-
-
-
additional information
?
-
-
ceramide kinase is a calcium-sensor
-
-
?
additional information
?
-
-
the enzyme is a mediator of calcium-dependent degranulation in mast cells
-
-
?
additional information
?
-
-
the enzyme forms intracellular complexes with calmodulin
-
-
?
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ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
ATP + ceramide
ADP + ceramide 1-phosphate
ATP + N-hexadecanoyl-sphingenine
ADP + N-hexadecanoyl-sphingenine 1-phosphate
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
additional information
?
-
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
-
-
-
?
ATP + C16-ceramide
ADP + C16-ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
ceramide is an important regulator of photoreceptor viability
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
ceramide 1-phosphate is a lipid signalling molecule involved in regulation of many physiological processes related to cell proliferation, apoptosis, and inflammation, most of them in concert with sphingosine 1-phosphate, ceramide 1-phosphate might act via extracellular cell surface receptors or intracellularly as second messenger
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
synthesis of the sphingolipid signaling molecule
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
-
-
?
ATP + ceramide
ADP + ceramide 1-phosphate
-
ceramide phosphorylation may be associated with neurotransmitter release
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CERK and its product Cer-1-P are implicated in signaling processes, Cer-1-P stimulates DNA synthesis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide is a key mediator of cellular apoptosis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is a critical mediator of eicosanoid synthesis, and its product, ceramide 1-phosphate, is required for the production of prostaglandins in response to several inflammatory agonists, CERK requires ceramide actively transported to the trans-Golgi network via ceramide transport protein CERT
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is important for cellular proliferation and survival, activation of cytosolic phospholipase A2, mast cell degranulation, and phagocytosis
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CERK and C1P are playing significant biological roles in cell-signaling cascades
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK has important roles in leukocyte functions, including the role in degranulation of mast cells and the phagocytosis of polymorphonuclear leukocytes
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
CERK plays a role in cell signalling
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
increased ceramide 1-phosphate during phagocytosis enhances phagocytosis and phagolysosome formation in COS-1 cells expressing hCERK
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
involvement in inflammatory processes and cell growth
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
key enzyme for controlling ceramide levels
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
-
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide 1-phosphate is a sphingolipid that participates in cell signaling, but ceramide kinase is not the only source of ceramide 1-phosphate
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
ceramide kinase is not the only source of ceramide 1-phosphate, ceramide kinase is important for neutrophil homeostasis, ceramide kinase is important for the defense against Streptococcus pneumoniae infections
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK and C1P are involved in many cell functions, including membrane fusion, phagocytosis and degranulation in mast cells
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK is not necessary for survival but might participate in neuronal functions involving emotional behavior
-
-
?
ceramide + ATP
ceramide 1-phosphate + ADP
-
CerK is involved in the regulation of mast cells
-
-
?
additional information
?
-
-
the enzyme does not play a role in neutrophil priming, the enzyme regulates the activity and translocalization of cytosolic phospholipase isozyme A2alpha, overview, the enzyme is involved in prostaglandin biosynthesis, i.e. intracellular arachidonic acid production, which is blocked by enzyme gene silencing
-
-
?
additional information
?
-
-
the enzyme is a critical mediator of eicosanoid synthesis
-
-
?
additional information
?
-
-
ceramide kinase is a calcium-sensor
-
-
?
additional information
?
-
-
the enzyme is a mediator of calcium-dependent degranulation in mast cells
-
-
?
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(4aR,6aS,12aS,12bR)-10-hydroxy-4,4,6a,12b-tetramethyl-1,3,4,4a,5,6,6a,12,12a,12b-decahydro-2H-benzo(a)xanthene-8,11-dione
-
KD, enantiomer of K1, strongly inhibits CerK activity
(4aS,6aR,12aR,12bS)-10-hydroxy-4,4,6a,12b-tetramethyl-1,3,4,4a,5,6,6a,12,12a,12b-decahydro-2H-benzo(a)xanthene-8,11-dione
1alpha,25-dihydroxyvitamin D3
enzyme activity decreases by approximately 40% in the presence of the hormone
2,5-dihydroxy-3-(((1R,4aR,8aR)-5,5,8a-trimethyl-2-methylidenedecahydronaphthalen-1-yl)methyl)cyclohexa-2,5-diene-1,4-dione
-
KB, enantiomer of K1, strongly inhibits CerK activity
2,5-dihydroxy-3-(((1S,2S,4aS,8aR)-2,5,5,8a-tetramethyldecahydronaphthalen-1-yl)methyl)cyclohexa-2,5-diene-1,4-dione
-
KC, F12509A with an additional hydrogen at the double bond in methylene position, weak inhibition
2,5-dihydroxy-3-(((1S,4aS,8aS)-5,5,8a-trimethyl-2-methylidenedecahydronaphthalen-1-yl)methyl)cyclohexa-2,5-diene-1,4-dione
-
F12509A, inhibitor of sphingosine kinase 1, weak inhibition
2,5-dihydroxy-3-[[(4aS,8aS)-2,5,5,8a-tetramethyl-3,4,4a,5,6,7,8,8a-octahydronaphthalen-1-yl]methyl]cyclohexa-2,5-diene-1,4-dione
-
K1, novel F-12509A olefin isomer, inhibitor decreases ceramide 1-phosphate levels without changing other lipids such as ceramide and sphingomyelin
3,3-cholamidopropyl-dimethylammonio-1-propanesulfonate
almost complete inhibition at high concentrations
3-(cyclohexylmethyl)-2,5-dihydroxycyclohexa-2,5-diene-1,4-dione
-
K2, cyclohexane derivative with a benzoquinone, weak inhibition
adamantane-1-carboxylic acid (2-benzoylamino-benzothiazol-6-yl)amide
-
NVP-231, a potent, specific, and reversible CerK inhibitor that competitively inhibits binding of ceramide to CerK
all-trans retinoic acid
inhibits ceramide kinase transkription in neuroblastoma cells
Ca2+
above 1 mM; inhibition above 1 mM
ceramide kinase inhibitor K1
-
-
D-erythro-N,N-dimethylsphingosine
-
dimethylsphingosine
-
DMS
F-12509A
0.1 mM, 40-50% inhibition, sphingosine kinase inhibitor
lauryldimethylammonium N-oxide
inhibitory at low concentrations
N,N-dimethylsphingosine
0.1 mM, 65% inhibition
N-acetyl-D-erythro-sphingenine
substrate inhibition above 0.1 mM
N-acetylsphingosine
-
i.e. C2-Cer, in vivo during inhibition of mast cell degranulation
N-ethyl-maleimide
thiol modifiying agent stops CerK acitivity, demonstrating that CerK contains exposed cysteine residues important for enzymatic activity
N-laurylsarcosine
inhibitory at low concentrations
N-[2-(benzoylamino)-6-benzothiazolyl]-tricyclo[3.3.1.13,7] decane-1-carboxamide
-
octyl-beta-D-glucopyranoside
almost complete inhibition at high concentrations
sphingosine
0.1 mM, 55% inhibition
W-7
-
calmodulin antagonist
ZK191784
enzyme activity decreases by approximately 25% in the presence of the hormone analogue
(4aS,6aR,12aR,12bS)-10-hydroxy-4,4,6a,12b-tetramethyl-1,3,4,4a,5,6,6a,12,12a,12b-decahydro-2H-benzo(a)xanthene-8,11-dione
ceramide kinase inhibitor K1, reduces the differences in degranulation observed between the bone marrow-derived mast cells from CERK-/- and wild-type mice in a dose-dependent manner
(4aS,6aR,12aR,12bS)-10-hydroxy-4,4,6a,12b-tetramethyl-1,3,4,4a,5,6,6a,12,12a,12b-decahydro-2H-benzo(a)xanthene-8,11-dione
-
K1, non-competitive, suppresses the activation of mast cells, strongly inhibits CerK activity
N-[2-(benzoylamino)-6-benzothiazolyl]-tricyclo[3.3.1.13,7] decane-1-carboxamide
NVP-231, a potent inhibitor of CerK
-
N-[2-(benzoylamino)-6-benzothiazolyl]-tricyclo[3.3.1.13,7] decane-1-carboxamide
NVP-231
-
NVP-231
diamino-benzothiazole derivative, potent inhibitor, no inhibition with its analog NVP-995
NVP-231
-
potent inhibition of ceramide kinase catalyzed production of ceramide 1-phosphate both in vitro and in cell-based assays
NVP-231
inhibits enzyme catalysis
NVP-231
inhibits enzyme catalysis
siRNA
-
downregulation of CerK with siRNA targeted against Cerk reduced cellular proliferation within 48 hours
-
siRNA
-
downregulation of CerK with siRNA targeted against Cerk reduced cellular proliferation within 48 hours
-
additional information
-
not inhibited by 1,2-diacylglycerol
-
additional information
no inhibition by ceramide analogues containing a carboxy group, i.e. N-acylated amino acids
-
additional information
-
no inhibition by ceramide analogues containing a carboxy group, i.e. N-acylated amino acids
-
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Adenocarcinoma
Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.
Adenocarcinoma of Lung
Activation of ceramidase and ceramide kinase by vanadate via a tyrosine kinase-mediated pathway.
Adenocarcinoma of Lung
Ceramide kinase regulates growth and survival of A549 human lung adenocarcinoma cells.
Asthma
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids.
Atherosclerosis
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids.
Breast Neoplasms
Ceramide Kinase Is Upregulated in Metastatic Breast Cancer Cells and Contributes to Migration and Invasion by Activation of PI 3-Kinase and Akt.
Breast Neoplasms
Ceramide kinase mediates intrinsic resistance and inferior response to chemotherapy in triple-negative breast cancer by upregulating Ras/ERK and PI3K/Akt pathways.
Breast Neoplasms
Ceramide kinase promotes tumor cell survival and mammary tumor recurrence.
Breast Neoplasms
Gene expression of ceramide kinase, galactosyl ceramide synthase and ganglioside GD3 synthase is associated with prognosis in breast cancer.
Carcinoma
Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.
Carcinoma, Lewis Lung
Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.
ceramide kinase deficiency
Ceramide kinase deficiency impairs microendothelial cell angiogenesis in vitro.
ceramide kinase deficiency
Ceramide kinase deficiency improves diet-induced obesity and insulin resistance.
Colitis
Knockout of Ceramide Kinase Aggravates Pathological and Lethal Responses in Mice with Experimental Colitis.
Cone-Rod Dystrophies
Expression and localization of CERKL in the mammalian retina, its response to light-stress, and relationship with NeuroD1 gene.
Hypersensitivity
Effect of eriodictyol on the development of atopic dermatitis-like lesions in ICR mice.
Hypersensitivity, Immediate
Effect of eriodictyol on the development of atopic dermatitis-like lesions in ICR mice.
Infections
Loss of ceramide kinase in Arabidopsis impairs defenses and promotes ceramide accumulation and mitochondrial H2O2 bursts.
Insulin Resistance
Ceramide kinase deficiency improves diet-induced obesity and insulin resistance.
Insulin Resistance
Serum Ceramide Kinase as a Biomarker of Cognitive Functions, and the Effect of Using Two Slimming Dietary Therapies in Obese Middle Aged Females.
Leukemia
Ceramide kinase expression is altered during macrophage-like cell differentiation of the leukemia cell line HL-60.
Leukemia
Characterization of a ceramide kinase activity from human leukemia (HL-60) cells. Separation from diacylglycerol kinase activity.
Lung Neoplasms
Inhibitory effects of ceramide kinase on Rac1 activation, lamellipodium formation, cell migration, and metastasis of A549 lung cancer cells.
Lung Neoplasms
The ceramide kinase inhibitor NVP-231 inhibits breast and lung cancer cell proliferation by inducing M phase arrest and subsequent cell death.
Muscular Atrophy
Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.
Neoplasm Metastasis
Inhibitory effects of ceramide kinase on Rac1 activation, lamellipodium formation, cell migration, and metastasis of A549 lung cancer cells.
Neoplasms
Alteration of Ceramide 1-O-Functionalization as a Promising Approach for Cancer Therapy.
Neoplasms
Ceramide kinase promotes tumor cell survival and mammary tumor recurrence.
Neoplasms
Ceramide kinase regulates the production of tumor necrosis factor ? (TNF?) via inhibition of TNF?-converting enzyme.
Neoplasms
Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase.
Neoplasms
Gene expression of ceramide kinase, galactosyl ceramide synthase and ganglioside GD3 synthase is associated with prognosis in breast cancer.
Neoplasms
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids.
Neoplasms
Regulation of cell growth, survival and migration by ceramide 1-phosphate - implications in lung cancer progression and inflammation.
Neoplasms
The Role of Ceramide 1-Phosphate in Tumor Cell Survival and Dissemination.
Neuroblastoma
ATRA inhibits ceramide kinase transcription in a human neuroblastoma cell line, SH-SY5Y cells: the role of COUP-TFI.
Neuroblastoma
Ceramide kinase regulates TNF?-stimulated NADPH oxidase activity and eicosanoid biosynthesis in neuroblastoma cells.
Neuroblastoma
New signalling pathway involved in the anti-proliferative action of vitamin D? and its analogues in human neuroblastoma cells. A role for ceramide kinase.
Obesity
Ceramide kinase deficiency improves diet-induced obesity and insulin resistance.
Obesity
Serum Ceramide Kinase as a Biomarker of Cognitive Functions, and the Effect of Using Two Slimming Dietary Therapies in Obese Middle Aged Females.
Pancreatic Neoplasms
Ceramide 1-phosphate regulates cell migration and invasion of human pancreatic cancer cells.
Respiratory Hypersensitivity
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids.
Retinal Degeneration
Hyperautofluorescent Dots are Characteristic in Ceramide Kinase Like-associated Retinal Degeneration.
Retinitis Pigmentosa
Expression and localization of CERKL in the mammalian retina, its response to light-stress, and relationship with NeuroD1 gene.
Retinitis Pigmentosa
Identification of a nuclear localization signal in the retinitis pigmentosa-mutated RP26 protein, ceramide kinase-like protein.
Retinitis Pigmentosa
Mutation of CERKL, a novel human ceramide kinase gene, causes autosomal recessive retinitis pigmentosa (RP26).
Starvation
Ceramide kinase regulates growth and survival of A549 human lung adenocarcinoma cells.
Thrombosis
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids.
Triple Negative Breast Neoplasms
Ceramide kinase mediates intrinsic resistance and inferior response to chemotherapy in triple-negative breast cancer by upregulating Ras/ERK and PI3K/Akt pathways.
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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
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
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
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
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
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
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
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
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
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
malfunction
miR-34a targets CERK resulting in ceramide accumulation, activation of PP2A and the pJNK pathway in muscle and C2C12 myoblasts. Overexpression of miR-34a in C2C12 myoblasts leads to alterations in the insulin signaling pathway, which are rescued by its antagonism
malfunction
treatment with ceramide kinase inhibitor K1, or nSMase inhibitor GW4869, decreases dopamine uptake in PC-12 cells, although the application of FB1, a ceramide synthase inhibitor, does not affect dopamine uptake. Transfection of nSMase2 and CERK siRNA decrease the dopamine transporter (DAT) surface level in PC-12 cells. SM-derived ceramide 1-phosphate affects cell surface levels of DAT. Protein-protein interaction between nSMase2 and DAT occur in the mouse striatum. Treatment of CERK knockdown PC-12 cells with C8-ceramide partially rescues the nSMase2 siRNA-induced decrease in DA uptake by about 40%, while treatment of C8-ceramide 1-phosphate also partially rescues the CERK sRNA-induced decrease in DA utake by about 45%
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
-
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
-
malfunction
-
treatment with ceramide kinase inhibitor K1, or nSMase inhibitor GW4869, decreases dopamine uptake in PC-12 cells, although the application of FB1, a ceramide synthase inhibitor, does not affect dopamine uptake. Transfection of nSMase2 and CERK siRNA decrease the dopamine transporter (DAT) surface level in PC-12 cells. SM-derived ceramide 1-phosphate affects cell surface levels of DAT. Protein-protein interaction between nSMase2 and DAT occur in the mouse striatum. Treatment of CERK knockdown PC-12 cells with C8-ceramide partially rescues the nSMase2 siRNA-induced decrease in DA uptake by about 40%, while treatment of C8-ceramide 1-phosphate also partially rescues the CERK sRNA-induced decrease in DA utake by about 45%
-
malfunction
-
miR-34a targets CERK resulting in ceramide accumulation, activation of PP2A and the pJNK pathway in muscle and C2C12 myoblasts. Overexpression of miR-34a in C2C12 myoblasts leads to alterations in the insulin signaling pathway, which are rescued by its antagonism
-
metabolism
-
sphingolipid metabolism
metabolism
functional role of the ASM/CERK pathway in cancer cell migration, and of the ASM/CERK signaling axis in cytokines associated with EMT, cell migration, and invasiveness
metabolism
involvement of the lysosome pathway in CerK levels and ceramide 1-phosphate formation
metabolism
myostatin (Mstn) and microRNA miR-34a antagonism can help ameliorate ceramide accumulation and loss of insulin sensitivity in aging skeletal muscle
metabolism
-
myostatin (Mstn) and microRNA miR-34a antagonism can help ameliorate ceramide accumulation and loss of insulin sensitivity in aging skeletal muscle
-
physiological function
-
ceramide kinase catalyzed formation of ceramide 1-phosphate may regulate angiogenesis by a novel mechanism that is independent of sphingosine-1-phosphate formation and signaling
physiological function
-
ceramide kinase, is a novel regulator of phosphoinositide-specific phospholipase C signaling and photoreceptor homeostasis, DCERK has a diacylglycerol kinase domain and a Ca2+/calmodulin binding domain
physiological function
enzyme plays an important role in cellular events such as cell growth and inflammation
physiological function
ceramide kinase might act as an modulator for mild and chronic activation of mast cells, thus increasing sensitivity to cytoplasmic Ca2+. CERK-/- mice are less prone to exhibiting a passive cutaneous anaphylactic shock-reaction compared to wild-type mice, the differences are not significant. In bone marrow-derived mast cells from CERK-/- mice activated by cross-linking antigen /IgE, low concentrations of Ag+ have a reduced effect on degranulation. Similarly, when the cells are activated with calcium ionophore to focus on the downstream signaling of Ca2+-elevation, only a low concentration of ionophore has a reduced effect on degranulation
physiological function
ceramide kinase/ceramide 1-phosphate axis acts as molecular effector of the anti-proliferative action of 1alpha,25-dihydroxyvitamin D3 and its analogues. The inhibition of ceramide kinase by specific gene silencing or pharmacological inhibition, drastically reduces cell proliferation. 1alpha,25-Dihydroxyvitamin D3 and structural analogue ZK191784 treatment induce a significant decrease in ceramide kinase expression and ceramide 1-phosphate content, and an increase of ceramide. The treatment of SH-SY5Y cells with ZK159222, antagonist of 1alpha,25-dihydroxyvitamin D3 receptor, trichostatin A, inhibitor of histone deacetylases, and COUP-TFI-siRNA prevents the decrease of ceramide kinase expression elicited by 1alpha,25-dihydroxyvitamin D3 supporting the involvement of VDR/COUP-TFI/histone deacetylase complex in ceramide kinase regulation
physiological function
a role for ceramide kinase in the production of eicosanoids. The initial rate-limiting step in eicosanoid biosynthesis is started by the activation of group IVA phospholipase A, 2cPLA2alpha, which is activated by direct binding of the C2 domain to ceramide-1-phosphate
physiological function
ceramide kinase catalyzes the generation of the sphingolipid ceramide-1-phosphate, which regulates various cellular functions including cell growth and death, and inflammation. Ceramide kinase contributes to proliferation but not to prostaglandin E2 formation in renal mesangial cells and fibroblasts
physiological function
ceramide kinase catalyzes the generation of the sphingolipid ceramide-1-phosphate, which regulates various cellular functions including cell growth and death, and inflammation. Ceramide kinase contributes to proliferation but not to prostaglandin E2 formation in renal mesangial cells and fibroblasts
physiological function
ceramide kinase promotes tumor cell survival and mammary tumor recurrence. Ceramide kinase is required for mammary tumor recurrence following HER2/neu pathway inhibition and is spontaneously upregulated during tumor recurrence in multiple genetically engineered mouse models for breast cancer. CERK expression is associated with an increased risk of recurrence in women with breast cancer, Cerk promotes tumor cell survival in vivo
physiological function
CERK is required for eicosanoid biosynthesis in response to mechanical insult. Proper migration of fibroblasts is one of the necessary steps of wound healing, requirement for the CERK-derived ceramide 1-phosphate in the proper healing response of wounds
physiological function
CERK is required for eicosanoid biosynthesis in response to mechanical insult. Simulation of mechanical trauma of a wound demonstrates steadily increasing levels of arachidonic acid in a time-dependent manner reflected in scratch-induced eicosanoid levels. Proper migration of fi broblasts is one of the necessary steps of wound healing, requirement for the CERK-derived ceramide 1-phosphate in the proper healing response of wounds
physiological function
phosphorylated sphingolipids ceramide-1-phosphate and sphingosine-1-phosphate are key regulators of cell growth, survival, migration, and inflammation. Ceramide 1-phosphate produced by ceramide kinase is an activator of group IVA cytosolic phospholipase A2alpha (cPLA2alpha), the rate-limiting releaser of arachidonic acid used for pro-inflammatory eicosanoid production, which contributes to disease pathogenesis in asthma/airway hyper-responsiveness, cancer, atherosclerosis, and thrombosis. To modulate eicosanoid action and avoid the damaging effects of chronic inflammation, cells require efficient targeting, trafficking, and presentation of ceramide 1-phosphate to specific cellular sites. Nonvesicular trafficking by a ceramide-1-phosphate transfer protein, CPTP, regulates eicosanoids, mechanism, overview. CPTP prevents excess ceramide-1-phosphate accumulation after production by CERK, thereby regulating cPLA2alpha action, diminishing arachidonic acid release and downstream generation of pro-inflammatory eicosanoids
physiological function
ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P). The activity of CerK is regulated by post-translational modifications including phosphorylation, CerK has a role in neuronal functions
physiological function
dopamine transporter trafficking is regulated by neutral sphingomyelinase 2/ceramide kinase (nSMase/CERK). The dopamine transporter (DAT) has an important role in the regulation of Dopamine (DA) reuptake. DAT recycling is regulated by ceramide kinase via the sphingomyelin pathway. Dopamine stimulates the formation of ceramide and increases nSMase activity in PC-12 cells, while treatment with a cell-permeable ceramide 1-phosphate (C1P) increases DA uptake. Endocytic recycling of DAT requires CERK
physiological function
endogenous bone marrow-derived mesenchymal stem cells (BM-MSCs) are mobilized into peripheral blood and injured tissues by various growth factors and cytokines that are expressed in the injured tissues, such as substance P (SP), stromal cell derived factor-1 (SDF-1), and transforming growth factor beta (TGF-beta). Extracellular bioactive lipid metabolites such as ceramide 1-phosphate and sphingosine 1-phosphate also modulate BM-MSC migration as SP, SDF-1, and TGF-beta. Ceramide kinase mediates the chemotactic migration of BM-MSCs in response to SP, SDF-1, or TGF-beta. Ceramide kinase regulates the migration of bone marrow-derived mesenchymal stem cells. The extracellular ceramide 1-phosphate regulates the migration of bone marrowderived multipotent mesenchymal stem cells (BM-MSCs) as well as macrophages, lung cancer cells, prostate cancer cells, and endothelial cells. Ceramide 1-phosphate generated by ceramide kinase is released extracellularly in order to induce cellular migration. Ceramide 1-phosphate also remains inside of cells in order to recruit cytosolic proteins and transduce signals. Ceramide kinase also regulates the expression of N-cadherin that is required for BM-MSCs migration induced by TGF-beta
physiological function
myostatin (Mstn) levels increase in aging mouse muscle and upregulate miR-34a, which inhibits CERK resulting in increased ceramide levels. This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4. These changes can result in reduced glucose uptake and insulin resistance. CERK inhibition affects insulin signaling pathway in C2C12 myoblasts via ceramide accumulation. CERK inhibition with NVP231 results in hypophosphorylation of insulin signaling molecules (PI3K, AKT, AS160, and GSK3b) and hyperphosphorylation of IRS1 (Ser307) when compared with dimethyl sulfoxide treated control C2C12 myoblasts
physiological function
TNF-alpha induces the formation of ceramide 1-phosphate (C-1-P) in a CERK-dependent manner. Silencing of CERK blocks CCL5 production in response to TNF-alpha. ASM and CERK induce a highly concordant program of cytokine production and both are required for migration of breast cancer cells. ASM can produce ceramide which is then converted to ceramide 1-phosphate by CERK, and that ceramide 1-phosphate is required for production of CCL5 and several cytokines and chemokines, with roles in cell migration. Enzyme CERK is required for CCL5 production and sufficient to induce CCL5 in MCF-7 breast cancer cells
physiological function
-
a role for ceramide kinase in the production of eicosanoids. The initial rate-limiting step in eicosanoid biosynthesis is started by the activation of group IVA phospholipase A, 2cPLA2alpha, which is activated by direct binding of the C2 domain to ceramide-1-phosphate
-
physiological function
-
CERK is required for eicosanoid biosynthesis in response to mechanical insult. Proper migration of fibroblasts is one of the necessary steps of wound healing, requirement for the CERK-derived ceramide 1-phosphate in the proper healing response of wounds
-
physiological function
-
dopamine transporter trafficking is regulated by neutral sphingomyelinase 2/ceramide kinase (nSMase/CERK). The dopamine transporter (DAT) has an important role in the regulation of Dopamine (DA) reuptake. DAT recycling is regulated by ceramide kinase via the sphingomyelin pathway. Dopamine stimulates the formation of ceramide and increases nSMase activity in PC-12 cells, while treatment with a cell-permeable ceramide 1-phosphate (C1P) increases DA uptake. Endocytic recycling of DAT requires CERK
-
physiological function
-
myostatin (Mstn) levels increase in aging mouse muscle and upregulate miR-34a, which inhibits CERK resulting in increased ceramide levels. This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4. These changes can result in reduced glucose uptake and insulin resistance. CERK inhibition affects insulin signaling pathway in C2C12 myoblasts via ceramide accumulation. CERK inhibition with NVP231 results in hypophosphorylation of insulin signaling molecules (PI3K, AKT, AS160, and GSK3b) and hyperphosphorylation of IRS1 (Ser307) when compared with dimethyl sulfoxide treated control C2C12 myoblasts
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C324A
same specific acitity as wild-type CerK
C398A
same specific acitity as wild-type CerK
CERKL
-
the point mutant enzyme CERKL does not phosphorylate ceramide or diacylglycerol and is localized in the nucleus
DELTA1-123
production by site-directed mutagenesis, localization in cytosol
DELTA124-537
production by site-directed mutagenesis, resulted in almost complete accumulation in the nucleus
DELTA219-496
production by site-directed mutagenesis, localization in cytosol and nucleus
DELTA340-537
production by site-directed mutagenesis, significant accumulation into the nucleus, existence of nuclear export signals in the C-terminal part of enzyme, traditional nuclear export signals 511-IEVRVHCQLVRL-522 in the CC3 domain and a class 2 nuclear export signals 347-CRAGCFVC-354 between the CC1 and the CC2 domains
DELTA454-537
production by site-directed mutagenesis, localization in cytosol and nucleus
DELTA514-537
production by site-directed mutagenesis, nuclear localization of ceramide kinase
DELTA520-537
production by site-directed mutagenesis, localization is mostly cytosolic but is also detected in the nucleus
DELTA525-537
production by site-directed mutagenesis, both localization and cellular activity are lost
DELTA528-537
production by site-directed mutagenesis, no effect of localization and activity when assaying at the cellular level with exogenously added substrate, activity is lost after cell lysis in vitro
DELTA533-537
production by site-directed mutagenesis, no effect of localization and activity
G2A
-
site-directed mutagenesis, reduced activity compared to the wild-type enzyme
K68A/K74A/K80A
shows wild type activity
K90V/K98V
shows partial activity
K90V/R91A
shows partial activity
K90V/R91A/R96A/K98V
totally devoid of activity
R29A/R33A/R36A
shows wild type activity
S340A
by site directed mutagenesis, using of Triton X-100 as lysis buffer results in 15% activity decrease in the mutant protein compared with the wild type enzyme, when octylglucoside is used instead of Triton X-100 for cell lysis, activity is reduced in the S340A mutant protein which reaches only 15% of wild type activity
S340D
by site directed mutagenesis, intermediate recovery of 16% is observed for the mutant protein
S427A
by site directed mutagenesis, activity in the S427A mutant protein amounts to only 30% of that of wild type enzyme
S427D
by site directed mutagenesis, mutant protein displays 50% of wild type activity
E8A
-
site-directed mutagenesis, the mutant shows unaltered activity compared to the wild-type enzyme
F429R
-
site-directed mutagenesis, weak binding of calmodulin compared to the wild-type enzyme
F431R
-
site-directed mutagenesis, no binding of calmodulin in contrary to the wild-type enzyme
G2A
-
site-directed mutagenesis, the mutant shows unaltered activity compared to the wild-type enzyme
L10A
-
site-directed mutagenesis, 99% reduced activity compared to the wild-type enzyme, substrate affinity and activation by Ca2+ are unaffected, mutation within the pleckstrin homology domain
L10I
-
site-directed mutagenesis, 71% reduced activity compared to the wild-type enzyme, substrate affinity and activation by Ca2+ are unaffected, mutation within the pleckstrin homology domain
L422R
-
site-directed mutagenesis, similar binding of calmodulin compared to the wild-type enzyme
L422R/F429R
-
site-directed mutagenesis
L435R
-
site-directed mutagenesis, no binding of calmodulin in contrary to the wild-type enzyme
P9A
-
site-directed mutagenesis, the mutant shows unaltered activity compared to the wild-type enzyme
S12A
-
site-directed mutagenesis, the mutant shows unaltered activity compared to the wild-type enzyme
C347A
lower specific acitity than wild-type CerK
C347A
by site-directed mutagenesis, mutation severely impairs localization at the Golgi complex resulting in cytosolic accumulation instead
C351A
lower specific acitity than wild-type CerK
C351A
by site-directed mutagenesis, mutation severely impairs localization at the Golgi complex resulting in cytosolic accumulation instead
C354A
by site-directed mutagenesis
C354A
lower specific acitity than wild-type CerK
additional information
generation of an 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. The effect of NaCl is partly dependent on the antagonistic interaction between endogenous abscisic acid (ABA) and salicylic acid (SA). The intact ABA pathway may not be required for this effect. The response of the acd5 mutant to abiotic stress shows that the mutants do not have the cell-death phenotype. 300 mM NaCl suppresses the cell-death phenotype of the acd5 mutant without inhibiting plant growth. NaCl treatment inhibits sphingolipid accumulation in the acd5 mutant and alters the endogenous levels of SA and ABA
additional information
a truncated mutant enzyme, lacking the first 115 amno acids, is not active and fails to be located in the plasma membrane
additional information
-
a truncated mutant enzyme, lacking the first 115 amno acids, is not active and fails to be located in the plasma membrane
additional information
-
siRNA to the gene encoding the enzyme for downregulation blocks arachidonic acid release and subsequent prostaglandin E2 production after stimulation
additional information
knockdown of CERK in MCF-7 cells by specific siRNA
additional information
knockdown of CerK is performed with shRNA to silence CerK (shCerK, target sequence GTT (TATCGAGTCAAGAAAT)). Establishment of a stable CerK-knockdown cell line (shCerK) and a HA-tagged CerK expressing cell line using a retroviral vector. Serum withdrawal causes ubiquitination of HA-tagged CerK protein and downregulates both HA-tagged CerK protein and ceramide 1-phosphate formation within 6 h, and these downregulations are abolished by co-treatments with NGF or proteasome inhibitors such as MG132 and clasto-lactacystin. Treatment with the proteasome inhibitors increases HA-tagged CerK in puncture structures, possibly endosomes and/or vesicles, in cells. Treatment with the lysosome inhibitors reduces serum withdrawal-induced downregulation of HA-tagged CerK protein but not ceramide 1-phosphate formation. 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. There is a positive correlation between noradrenaline release and formation of ceramide 1-phosphate and/or HA-tagged CerK levels in NGF- and clasto-lactacystin-treated cells
additional information
-
construction of an enzyme mutant which shows loss of activity but contains the calmodulin binding motif, expression of the mutant inhibits Ca2+-dependent ceramide 1-phosphate formation
additional information
-
construction of N-terminally truncated mutants lacking the first 7, 12, or 76 amino acid residues, respectively, mutant DELTAN7 is still active while mutants DELTAN12 and DELTAN76 are catalytically inactive
additional information
construction of CerK knockout cells
additional information
generation of CERK-/- knockout mice
additional information
generation of CERK-/- knockout mice and enzyme silencing by siRNA
additional information
-
generation of CERK-/- knockout mice and enzyme silencing by siRNA
additional information
-
generation of CERK-/- knockout mice and enzyme silencing by siRNA
-
additional information
-
generation of CERK-/- knockout mice
-
additional information
construction of CerK knockout cells
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A conserved cysteine motif essential for ceramide kinase function
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Homo sapiens
brenda
Murakami, M.; Ito, H.; Hagiwara, K.; Yoshida, K.; Sobue, S.; Ichihara, M.; Takagi, A.; Kojima, T.; Tanaka, K.; Tamiya-Koizumi, K.; Kyogashima, M.; Suzuki, M.; Banno, Y.; Nozawa, Y.; Murate, T.
ATRA inhibits ceramide kinase transcription in a human neuroblastoma cell line, SH-SY5Y cells: The role of COUP-TFI
J. Neurochem.
112
511-520
2010
Homo sapiens (Q8TCT0), Homo sapiens
brenda
Chen, W.Q.; Graf, C.; Zimmel, D.; Rovina, P.; Krapfenbauer, K.; Jaritz, M.; Parker, P.J.; Lubec, G.; Bornancin, F.
Ceramide kinase profiling by mass spectrometry reveals a conserved phosphorylation pattern downstream of the catalytic site
J. Proteome Res.
9
420-429
2010
Homo sapiens (Q8TCT0)
brenda
Niwa, S.; Graf, C.; Bornancin, F.
Ceramide kinase deficiency impairs microendothelial cell angiogenesis in vitro
Microvasc. Res.
77
389-393
2009
Mus musculus
brenda
Dasgupta, U.; Bamba, T.; Chiantia, S.; Karim, P.; Tayoun, A.N.; Yonamine, I.; Rawat, S.S.; Rao, R.P.; Nagashima, K.; Fukusaki, E.; Puri, V.; Dolph, P.J.; Schwille, P.; Acharya, J.K.; Acharya, U.
Ceramide kinase regulates phospholipase C and phosphatidylinositol 4, 5, bisphosphate in phototransduction
Proc. Natl. Acad. Sci. USA
106
20063-20068
2009
Drosophila melanogaster
brenda
Bini, F.; Frati, A.; Garcia-Gil, M.; Battistini, C.; Granado, M.; Martinesi, M.; Mainardi, M.; Vannini, E.; Luzzati, F.; Caleo, M.; Peretto, P.; Gomez-Munoz, A.; Meacci, E.
New signalling pathway involved in the anti-proliferative action of vitamin D3 and its analogues in human neuroblastoma cells. A role for ceramide kinase
Neuropharmacology
63
524-537
2012
Homo sapiens (Q8TCT0), Homo sapiens
brenda
Mitsutake, S.; Kumada, H.; Soga, M.; Hurue, Y.; Asanuma, F.; Nagira, M.; Deguchi, M.; Date, T.; Yokose, U.; Inagaki, Y.; Sugiura, M.; Kohama, T.; Igarashi, Y.
Ceramide kinase is not essential but might act as an Ca2+-sensor for mast cell activation
Prostaglandins Other Lipid Mediat.
93
109-112
2010
Mus musculus (Q8K4Q7)
brenda
Payne, A.W.; Pant, D.K.; Pan, T.C.; Chodosh, L.A.
Ceramide kinase promotes tumor cell survival and mammary tumor recurrence
Cancer Res.
74
6352-6363
2014
Homo sapiens (Q8TCT0), Homo sapiens
brenda
Pastukhov, O.; Schwalm, S.; Roemer, I.; Zangemeister-Wittke, U.; Pfeilschifter, J.; Huwiler, A.
Ceramide kinase contributes to proliferation but not to prostaglandin E2 formation in renal mesangial cells and fibroblasts
Cell. Physiol. Biochem.
34
119-133
2014
Rattus norvegicus (D3Z9Y3), Mus musculus (Q8K4Q7)
brenda
Mietla, J.A.; Wijesinghe, D.S.; Hoeferlin, L.A.; Shultz, M.D.; Natarajan, R.; Fowler, A.A.; Chalfant, C.E.
Characterization of eicosanoid synthesis in a genetic ablation model of ceramide kinase
J. Lipid Res.
54
1834-1847
2013
Mus musculus (Q8K4Q7), Mus musculus, Mus musculus BALB/c (Q8K4Q7)
brenda
Wijesinghe, D.S.; Brentnall, M.; Mietla, J.A.; Hoeferlin, L.A.; Diegelmann, R.F.; Boise, L.H.; Chalfant, C.E.
Ceramide kinase is required for a normal eicosanoid response and the subsequent orderly migration of fibroblasts
J. Lipid Res.
55
1298-1309
2014
Mus musculus (Q8K4Q7), Homo sapiens (Q8TCT0), Homo sapiens, Mus musculus BALB/c (Q8K4Q7)
brenda
Simanshu, D.K.; Kamlekar, R.K.; Wijesinghe, D.S.; Zou, X.; Zhai, X.; Mishra, S.K.; Molotkovsky, J.G.; Malinina, L.; Hinchcliffe, E.H.; Chalfant, C.E.; Brown, R.E.; Patel, D.J.
Non-vesicular trafficking by a ceramide-1-phosphate transfer protein regulates eicosanoids
Nature
500
463-467
2013
Homo sapiens (Q8TCT0), Homo sapiens
brenda
Yu, J.; Kim, H.M.; Kim, K.P.; Son, Y.; Kim, M.S.; Park, K.S.
Ceramide kinase regulates the migration of bone marrow-derived mesenchymal stem cells
Biochem. Biophys. Res. Commun.
508
361-367
2019
Mus musculus (Q8K4Q7)
brenda
Hori, M.; Gokita, M.; Yasue, M.; Honda, T.; Kohama, T.; Mashimo, M.; Nakamura, H.; Murayama, T.
Down-regulation of ceramide kinase via proteasome and lysosome pathways in PC12 cells by serum withdrawal its protection by nerve growth factor and role in exocytosis
Biochim. Biophys. Acta
1867
118714
2020
Homo sapiens (Q8TCT0)
brenda
Won, J.H.; Kim, S.K.; Shin, I.C.; Ha, H.C.; Jang, J.M.; Back, M.J.; Kim, D.K.
Dopamine transporter trafficking is regulated by neutral sphingomyelinase 2/ceramide kinase
Cell. Signal.
44
171-187
2018
Mus musculus (Q8K4Q7), Mus musculus, Mus musculus C57BL/6 (Q8K4Q7)
brenda
Kukreti, H.; Amuthavalli, K.
MicroRNA-34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase (CERK) in aging skeletal muscle
J. Cell. Biochem.
121
3070-3089
2020
Mus musculus (Q8K4Q7), Mus musculus, Mus musculus C57BL/6J (Q8K4Q7)
brenda
Newcomb, B.; Rhein, C.; Mileva, I.; Ahmad, R.; Clarke, C.J.; Snider, J.; Obeid, L.M.; Hannun, Y.A.
Identification of an acid sphingomyelinase ceramide kinase pathway in the regulation of the chemokine CCL5
J. Lipid Res.
59
1219-1229
2018
Homo sapiens (Q8TCT0)
brenda
Yang, Y.B.; Yin, J.; Huang, L.Q.; Li, J.; Chen, D.K.; Yao, N.
Salt enhances disease resistance and suppresses cell death in ceramide kinase mutants
Plant Physiol.
181
319-331
2019
Arabidopsis thaliana (Q6USK2)
brenda