Literature summary for 3.1.4.3 extracted from

Erttmann, S.F.; Gekara, N.O.; Faellman, M.
Bacteria induce prolonged PMN survival via a phosphatidylcholine-specific phospholipase C- and protein kinase C-dependent mechanism (2014), PLoS ONE, 9, e87859.

Search for more literature for 3.1.4.3

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
polymorphonuclear leukocyte	from peripheral blood	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
PC-PLC	-	Homo sapiens
phosphatidylcholine-specific phospholipase C	-	Homo sapiens

General Information

General Information	Comment	Organism
malfunction	inhibition of the enzyme abrogates the Yersinia pseudotuberculosis-induced repression of caspase 3 activity	Homo sapiens
metabolism	protein kinase C and phosphatidylcholine-specific phospholipase C, but not tyrosine kinases or phosphatidylinositol-specific phospholipase C are key players in this dual polymorphonuclear leukocyte response to bacterial infection, e.g. by Yersinia pseudotuberculosis, Escherichia coli, or Staphylococcus aureus, and by pro-inflammatory cytokine production including interleukin-8 and tumor necrosis factor-alpha	Homo sapiens
physiological function	the enzyme signaling is required for polymorphonuclear leukocyte survival after bacterial infection and Toll-like receptor-mediated induction of interleukin-8 and TNFalpha gene expression. The enzyme activity is involved in bacteria-mediated suppression of caspase 3 activity	Homo sapiens

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Release 2023.1 (January 2023)