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Nat Genet. 1997 Aug;16(4):358-63.

Bcl-2 and Bax function independently to regulate cell death.

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Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USA.


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 Bax and Bcl-2, each is able to regulate apoptosis independently.

[Indexed for MEDLINE]

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