Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak (original) (raw)

Nature volume 374, pages 736–739 (1995)Cite this article

Abstract

MEMBERSof the Bcl-2 family of proteins are characterized by their ability to modulate cell death. Bcl-2 and some of its homologues inhibit apoptosis1–4, whereas other family members, such as Bax, will accelerate apoptosis under certain conditions5. Here we describe the identification and characterization of a complementary DNA that encodes a previously unknown Bcl-2 homologue designated Bak. Like Bax, the bak gene product primarily enhances apoptotic cell death following an appropriate stimulus. Unlike Bax, however, Bak can inhibit cell death in an Epstein–Barr-virus-transformed cell line. The widespread tissue distribution of Bak messenger RNA, including those containing long-lived, terminally differentiated cell types, suggests that cell-death-inducing activity is broadly distributed, and that tissue-specific modulation of apoptosis is controlled primarily by regulation of molecules that inhibit apoptosis.

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Authors and Affiliations

  1. LXR Biotechnology Inc., 1401 Marina Way South, Richmond, California, 94804, USA
    Michael C. Kiefer, Matthew J. Brauer, Virginia C. Powers, Jason J. Wu, Samuil R. Umansky, L. David Tomei & Philip J. Barr

Authors

  1. Michael C. Kiefer
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  2. Matthew J. Brauer
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  3. Virginia C. Powers
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  4. Jason J. Wu
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  5. Samuil R. Umansky
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  6. L. David Tomei
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  7. Philip J. Barr
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Kiefer, M., Brauer, M., Powers, V. et al. Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak.Nature 374, 736–739 (1995). https://doi.org/10.1038/374736a0

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