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Modulation of apoptosis by the widely distributed Bcl-2 homologueBak

Identifieur interne : 003360 ( Main/Exploration ); précédent : 003359; suivant : 003361

Modulation of apoptosis by the widely distributed Bcl-2 homologueBak

Auteurs : Michael C. Kiefer [États-Unis] ; Matthew J. Brauer [États-Unis] ; Virginia C. Powers [États-Unis] ; Jason J. Wu [États-Unis] ; Samuil R. Umansky [États-Unis] ; L. David Tomei [États-Unis] ; Philip J. Barr [États-Unis]

Source :

RBID : ISTEX:03F0F75E768E486A086B5B81397EA49846795CFE

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 apoptosis14, 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 EpsteinBarr-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.

Url:
DOI: 10.1038/374736a0


Affiliations:


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