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Literature summary for 2.7.1.138 extracted from

  • 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 (2018), J. Lipid Res., 59, 1219-1229 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.1.138

Protein Variants

Protein Variants Comment Organism
additional information knockdown of CERK in MCF-7 cells by specific siRNA Homo sapiens

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + ceramide Homo sapiens
-
 ADP + ceramide 1-phosphate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q8TCT0
-
-

Source Tissue

Source Tissue Comment Organism Textmining
breast cancer cell
-
 Homo sapiens
-
MCF-7 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + ceramide
-
 Homo sapiens ADP + ceramide 1-phosphate
-
 ?

Synonyms

Synonyms Comment Organism
CERK
-
 Homo sapiens

Cofactor

Cofactor Comment Organism Structure
ATP
-
 Homo sapiens

General Information

General Information Comment Organism
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 Homo sapiens
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 Homo sapiens
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 Homo sapiens