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Literature summary for 3.1.1.4 extracted from
- Taiwan cobra phospholipase A2-elicited JNK activation is responsible for autocrine fas-mediated cell death and modulating Bcl-2 and Bax protein expression in human leukemia K562 cells (2010), J. Cell. Biochem., 109, 245-254.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Naja atra | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| venom | - |
Naja atra | - |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| phospholipase A2 | - |
Naja atra |
| PLA2 | - |
Naja atra |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | induces apoptotic death of human leukemia K562 cells in a concentration- and time-dependent manner. Degradation of procaspases, production of tBid, loss of mitochondrial membrane potential, Bcl-2 degradation, mitochondrial translocation of Bax, and cytochrome c release in PLA2-treated cells. PLA2 treatment increases Fas and FasL protein expression and activates p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun NH2-terminal kinase) in K562 cells. SB202190 pretreatment promotes the cytotoxic effect of PLA2 toward K562 cells in a time-dependent manner. SP600125 (JNK inhibitor) abolishes the cytotoxic effect of PLA2 and PLA2-induced autocrine Fas death pathway | Naja atra |
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Release 2023.1 (January 2023)
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