Title : How protein kinase C activation protects nerve cells from oxidative stress-induced cell death.

Pub. Date : 2001 May 1

PMID : 11312276






3 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 TPA treatment leads to the rapid activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), the inactivation of p38 mitogen-activated protein kinase (MAPK), and the downregulation of PKCdelta. Tetradecanoylphorbol Acetate mitogen-activated protein kinase 8 Homo sapiens
2 TPA treatment leads to the rapid activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), the inactivation of p38 mitogen-activated protein kinase (MAPK), and the downregulation of PKCdelta. Tetradecanoylphorbol Acetate mitogen-activated protein kinase 8 Homo sapiens
3 Both p38 MAPK inactivation and JNK activation appear to be downstream of ERK because an agent that blocks ERK activation also blocks the modulation of these other MAP kinase family members by TPA treatment. Tetradecanoylphorbol Acetate mitogen-activated protein kinase 8 Homo sapiens