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.
journal_name
Celljournal_title
Cellauthors
Oltvai ZN,Milliman CL,Korsmeyer SJdoi
10.1016/0092-8674(93)90509-osubject
Has Abstractpub_date
1993-08-27 00:00:00pages
609-19issue
4eissn
0092-8674issn
1097-4172pii
0092-8674(93)90509-Ojournal_volume
74pub_type
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