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Article

Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

27 Apr 2001

Abstract excerpt

Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells...

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Identifiers

PMID: 11326099
DOI: 10.1126/science.1059108

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Related research

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Research trail→

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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and DeathPMID 11326099Read ↗

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DRP1-dependent apoptotic mitochondrial fission occurs independently of BAX, BAK and APAF1 to amplify cell death by BID and oxidative stressSemantic proximity Read ↗

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Physiological and Pharmacological Control of BAK, BAX, and BeyondSemantic proximity Read ↗

Structure-function comparisons of the proapoptotic protein Bax in yeast and mammalian cells.Semantic proximity Read ↗

The deadly landscape of pro‐apoptotic BCL ‐2 proteins in the outer mitochondrial membraneSemantic proximity Read ↗

A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis.Semantic proximity Read ↗

Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak.Semantic proximity Read ↗

Interrelated roles for Mcl-1 and BIM in regulation of TRAIL-mediated mitochondrial apoptosis.Semantic proximity Read ↗

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