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Literature summary extracted from

  • Mullen, T.D.; Jenkins, R.W.; Clarke, C.J.; Bielawski, J.; Hannun, Y.A.; Obeid, L.M.
    Ceramide synthase-dependent ceramide generation and programmed cell death involvement of salvage pathway in regulating postmitochondrial events (2011), J. Biol. Chem., 286, 15929-15942 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
2.3.1.24 gene CERS5, quantitative real-time PCR enzyme expression analysis Homo sapiens
2.3.1.24 gene CERS6, quantitative real-time PCR enzyme expression analysis Homo sapiens
2.3.1.297 gene CERS2, quantitative real-time PCR enzyme expression analysis Homo sapiens
2.3.1.299 gene CERS1, quantitative real-time PCR enzyme expression analysis Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
2.3.1.24 fumonisin B1 inhibits the increase in total cellular ceramide induced by UV-C irradiation; inhibits the increase in total cellular ceramide induced by UV-C irradiation Homo sapiens
2.3.1.297 fumonisin B1 inhibits the increase in total cellular ceramide induced by UV-C irradiation Homo sapiens
2.3.1.299 fumonisin B1 inhibits the increase in total cellular ceramide induced by UV-C irradiation Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
2.3.1.24 microsome
-
 Homo sapiens
-
-
2.3.1.297 microsome
-
 Homo sapiens
-
-
2.3.1.299 microsome
-
 Homo sapiens
-
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.3.1.24 sphingosine + palmitoyl-CoA Homo sapiens
-
 N-palmitoylsphingosine + CoA
-
 ?
2.3.1.297 sphingosine + stearoyl-CoA Homo sapiens
-
 N-stearoylsphingosine + CoA
-
 ?
2.3.1.299 sphingosine + stearoyl-CoA Homo sapiens
-
 N-stearoylsphingosine + CoA
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
2.3.1.24 Homo sapiens Q6ZMG9
-
-
2.3.1.24 Homo sapiens Q8N5B7
-
-
2.3.1.297 Homo sapiens Q96G23
-
-
2.3.1.299 Homo sapiens P27544
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
2.3.1.24 breast adenocarcinoma cell
-
 Homo sapiens
-
2.3.1.24 HeLa cell
-
 Homo sapiens
-
2.3.1.24 MCF-7 cell
-
 Homo sapiens
-
2.3.1.24 MCF-7 cell CerS2 and CerS6 are the major very long-chain and long-chain CerS isoforms in MCF-7 cells, respectively Homo sapiens
-
2.3.1.297 breast adenocarcinoma cell
-
 Homo sapiens
-
2.3.1.297 HeLa cell
-
 Homo sapiens
-
2.3.1.297 MCF-7 cell CerS2 and CerS6 are the major very long-chain and long-chain CerS isoforms in MCF-7 cells, respectively Homo sapiens
-
2.3.1.299 breast adenocarcinoma cell
-
 Homo sapiens
-
2.3.1.299 HeLa cell
-
 Homo sapiens
-
2.3.1.299 MCF-7 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.3.1.24 sphingosine + palmitoyl-CoA
-
 Homo sapiens N-palmitoylsphingosine + CoA
-
 ?
2.3.1.297 sphingosine + stearoyl-CoA
-
 Homo sapiens N-stearoylsphingosine + CoA
-
 ?
2.3.1.299 sphingosine + stearoyl-CoA
-
 Homo sapiens N-stearoylsphingosine + CoA
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.3.1.24 C16:0-CerS
-
 Homo sapiens
2.3.1.24 ceramide synthase 5
-
 Homo sapiens
2.3.1.24 ceramide synthase 6
-
 Homo sapiens
2.3.1.24 CerS5
-
 Homo sapiens
2.3.1.24 CerS6
-
 Homo sapiens
2.3.1.297 ceramide synthase 2
-
 Homo sapiens
2.3.1.297 CerS2
-
 Homo sapiens
2.3.1.299 ceramide synthase 1
-
 Homo sapiens
2.3.1.299 CerS1
-
 Homo sapiens

Temperature Optimum [°C]

EC Number Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
2.3.1.24 37
-
 assay at Homo sapiens
2.3.1.297 37
-
 assay at Homo sapiens
2.3.1.299 37
-
 assay at Homo sapiens

pH Optimum

EC Number pH Optimum Minimum pH Optimum Maximum Comment Organism
2.3.1.24 7.4
-
 assay at Homo sapiens
2.3.1.297 7.4
-
 assay at Homo sapiens
2.3.1.299 7.4
-
 assay at Homo sapiens

Expression

EC Number Organism Comment Expression
2.3.1.24 Homo sapiens UV-C irradiation decreases the expression of CerS5 enzyme by about 50% down
2.3.1.297 Homo sapiens UV-C irradiation increases the enzyme expression by 1.27fold up
2.3.1.299 Homo sapiens UV-C irradiation increases the CerS1 enzyme expression by 1.27fold up

General Information

EC Number General Information Comment Organism
2.3.1.24 malfunction inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Combined knockdown of CerS5 and CerS6 is able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation, CerS6 knockdown clearly decreases C14:0- and C16:0-Cer basally and reduces their accumulation following UV-C irradiation, CerS5 knockdown has no appreciable effects on Cer levels. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells Homo sapiens
2.3.1.24 malfunction inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Combined knockdown of CerS5 and CerS6 is able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation, knockdown of CerS6 actually even increases total ceramide levels. CerS5 knockdown has no appreciable effects on Cer levels. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells Homo sapiens
2.3.1.24 metabolism regulation of sphingolipid metabolism by UV-C irradiation, overview. Ceramide species that are the least abundant (e.g. C18-Cer, C18:1-Cer, C20-Cer, C22:1-Cer, etc.) exhibit the greatest fold increases. More abundant ceramide species (e.g. C16-Cer, C24-Cer, and C24:1-Cer) show more modest fold changes, although they account for much more of the overall increase in ceramides Homo sapiens
2.3.1.24 physiological function sphingolipid ceramides are widely implicated in the regulation of programmed cell death or apoptosis. CerS5 and CerS6 regulate C16:0-Cer synthesis. Ceramide synthase inhhibitor fumonisin B1 inhibits cell death, suggesting the presence of a ceramide synthase (CerS)-dependent, sphingosine-derived pool of ceramide in regulating programmed cell death. This pool does not regulate the mitochondrial pathway, but it partially regulates activation of caspase-7 and is necessary for late plasma membrane permeabilization. Mechanisms of its generation and regulatory role during apoptosis, overview Homo sapiens
2.3.1.297 malfunction inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation. Knockdown of CerS2 in untreated cells reduces very long-chain Cer and increases long-chain Cer both in untreated and UV-C-treated cells. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells Homo sapiens
2.3.1.297 metabolism regulation of sphingolipid metabolism by UV-C irradiation, overview. Ceramide species that are the least abundant (e.g. C18-Cer, C18:1-Cer, C20-Cer, C22:1-Cer, etc.) exhibit the greatest fold increases. More abundant ceramide species (e.g. C16-Cer, C24-Cer, and C24:1-Cer) show more modest fold changes, although they account for much more of the overall increase in ceramides Homo sapiens
2.3.1.297 physiological function sphingolipid ceramides are widely implicated in the regulation of programmed cell death or apoptosis. CerS2 regulates very long-chain Cer synthesis. CerS2 and CerS6 are the major very long-chain and long-chain CerS isoforms in MCF-7 cells, respectively Homo sapiens
2.3.1.299 malfunction inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation. CerS1 knockdown has minimal effects in untreated cells and fails to prevent the accumulation of any Cer species following irradiation. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells Homo sapiens
2.3.1.299 metabolism regulation of sphingolipid metabolism by UV-C irradiation, overview. Ceramide species that are the least abundant (e.g. C18-Cer, C18:1-Cer, C20-Cer, C22:1-Cer, etc.) exhibit the greatest fold increases. More abundant ceramide species (e.g. C16-Cer, C24-Cer, and C24:1-Cer) show more modest fold changes, although they account for much more of the overall increase in ceramides Homo sapiens
2.3.1.299 physiological function sphingolipid ceramides are widely implicated in the regulation of programmed cell death or apoptosis. CerS1 regulates C18:0-Cer synthesis Homo sapiens