The Bax subfamily of Bcl2-related proteins is essential for apoptotic signal transduction by c-Jun NH2-terminal kinase

Kui Lei, Anjaruwee Nimnual, Wei Xing Zong, Norman J. Kennedy, Richard A. Flavell, Craig B. Thompson, Dafna Bar-Sagi, Roger J. Davis

Research output: Contribution to journalArticlepeer-review

430 Scopus citations

Abstract

Targeted gene disruption studies have established that the c-Jun NH2-terminal kinase (JNK) signaling pathway is required for stress-induced release of mitochondrial cytochrome c and apoptosis. Here we demonstrate that activated JNK is sufficient to induce rapid cytochrome c release and apoptosis. However, activated JNK fails to cause death in cells deficient of members of the Bax subfamily of proapoptotic Bcl2-related proteins. Furthermore, exposure to stress fails to activate Bax, cause cytochrome c release, and induce death in JNK-deficient cells. These data demonstrate that proapoptotic members of the Bax protein subfamily are essential for JNK-dependent apoptosis.

Original languageEnglish (US)
Pages (from-to)4929-4942
Number of pages14
JournalMolecular and cellular biology
Volume22
Issue number13
DOIs
StatePublished - 2002
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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