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Cell. 1993 Aug 27;74(4):609-19.

Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death.

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  • 1Howard Hughes Medical Institute Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

Abstract

Bcl-2 protein is able to repress a number of apoptotic death programs. To investigate the mechanism of Bcl-2's effect, we examined whether Bcl-2 interacted with other proteins. We identified an associated 21 kd protein partner, Bax, that has extensive amino acid homology with Bcl-2, focused within highly conserved domains I and II. Bax is encoded by six exons and demonstrates a complex pattern of alternative RNA splicing that predicts a 21 kd membrane (alpha) and two forms of cytosolic protein (beta and gamma). Bax homodimerizes and forms heterodimers with Bcl-2 in vivo. Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line. Overexpressed Bax also counters the death repressor activity of Bcl-2. These data suggest a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.

PMID:
8358790
[PubMed - indexed for MEDLINE]

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