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Bcl-2 and Bax function independently to regulate cell death

Nature Genetics volume 16, pages 358–363 (1997)Cite this article

Abstract

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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Authors and Affiliations

  1. The Howard Hughes Medical Institute and the Division of Molecular Oncology, Departments of Medicine and Pathology, Washington University School of Medicine, St. Louis, Missouri, 63110, USA

    C. Michael Knudson & Stanley J. Korsmeyer

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  1. C. Michael Knudson
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  2. Stanley J. Korsmeyer
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Knudson, C., Korsmeyer, S. Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16, 358–363 (1997). https://doi.org/10.1038/ng0897-358

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