| First Author | Kiefer MC | Year | 1995 |
| Journal | Nature | Volume | 374 |
| Issue | 6524 | Pages | 736-9 |
| PubMed ID | 7715731 | Mgi Jnum | J:43661 |
| Mgi Id | MGI:1098204 | Doi | 10.1038/374736a0 |
| Citation | Kiefer MC, et al. (1995) Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak. Nature 374(6524):736-9 |
| abstractText | Members of the Bcl-2 family of proteins are characterized by their ability to modulate cell death. Bcl-2 and some of its homologues inhibit apoptosis, whereas other family members, such as Bax, will accelerate apoptosis under certain conditions. 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. |
