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Title:
Bcl-2 and Bax function independently to regulate cell death | Nature Genetics
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The BCL-2 family has various pairs of antagonist and agonist proteins that regulate apoptosis. Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2–deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between fiaxand Bax and Bcl-2, each is able to regulate apoptosis independently.
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nature portfolio permissions reprints privacy policy advertising social media nature 335 nature 369 nature 379 nature 356 nature 381 nature 348 nature amyloid beta1–42-induced apoptosis b-cell neoplasms result personal data bax-induced cell death data protection permissions springerlink instant access promotes thymocyte differentiation murine development bcl-xl function upstream fas-induced activation cell death pathway—bcl-2 mitochondrial membrane protein development privacy immature hematopoietic cells ice protease cascade promotes cell death bcl-2 protein family bcl-2 family proteins programmed cell death protein binding functions explore content subscription content michael knudson & stanley european economic area thymic hypoplasia characteristic institutional subscriptions read transcriptionally active locus distorted small intestine trophic factor deprivation cd4+cd8+ stage washington university school chicken manure amendment statistical experimental designs colon cancer gaber defined neuroprotective agent bcl-2 protein expression
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