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Literature summary for 1.5.1.6 extracted from

  • Ghose, S.; Oleinik, N.V.; Krupenko, N.I.; Krupenko, S.A.
    10-formyltetrahydrofolate dehydrogenase-induced c-Jun-NH2-kinase pathways diverge at the c-Jun-NH2-kinase substrate level in cells with different p53 status (2009), Mol. Cancer Res., 7, 99-107.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
A-549 cell
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Homo sapiens
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PC-3 cell
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Homo sapiens
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General Information

General Information Comment Organism
physiological function FDH induces apoptosis in PC-3 prostate cells through simultaneous activation of the c-Jun-NH2-kinase JNK and extracellular signal-regulated kinase ERK pathways with JNK phosphorylating c-Jun and ERK1/2 phosphorylating Elk-1. The JNK1/2 inhibitor SP600125 or ERK1/2 inhibitor PD98059 prevents phosphorylation of c-Jun and Elk-1, correspondingly and partially protects PC-3 cells from FDH-induced cytotoxicity. Combination of the two inhibitors produces an additive effect. The FDH-induced apoptosis in p53-proficient A-549 cells also proceeds through activation of JNK1/2, but the down-stream target for JNK2 is p53 instead of c-Jun. In A-549 cells, FDH activates caspase 9, whereas in PC-3 cells, it activates caspase 8 Homo sapiens