JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins

Targeted gene disruption studies have established that the c-Jun NH(2)-terminal kinase (JNK) is required for the stress-induced release of mitochondrial cytochrome c and apoptosis, and that the Bax subfamily of Bcl-2-related proteins is essential for JNK-dependent apoptosis. However, the mechanism b...

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Veröffentlicht in:	EMBO J
Hauptverfasser:	Tsuruta, Fuminori, Sunayama, Jun, Mori, Yasunori, Hattori, Seisuke, Shimizu, Shigeomi, Tsujimoto, Yoshihide, Yoshioka, Katsuji, Masuyama, Norihisa, Gotoh, Yukiko
Format:	Artigo
Sprache:	Inglês
Veröffentlicht:	Nature Publishing Group 2004
Schlagworte:	Article
Online-Zugang:	https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC394248/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/15071501/ https://ncbi.nlm.nih.govhttps://doi.org/10.1038/sj.emboj.7600194
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JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins

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