| First Author | Knudson CM | Year | 1997 |
| Journal | Nat Genet | Volume | 16 |
| Issue | 4 | Pages | 358-63 |
| PubMed ID | 9241272 | Mgi Jnum | J:42051 |
| Mgi Id | MGI:894988 | Doi | 10.1038/ng0897-358 |
| Citation | Knudson CM, et al. (1997) Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16(4):358-63 |
| abstractText | 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. |
