| First Author | Chao DT | Year | 1995 |
| Journal | J Exp Med | Volume | 182 |
| Issue | 3 | Pages | 821-8 |
| PubMed ID | 7650488 | Mgi Jnum | J:78583 |
| Mgi Id | MGI:2385423 | Doi | 10.1084/jem.182.3.821 |
| Citation | Chao DT, et al. (1995) Bcl-XL and Bcl-2 repress a common pathway of cell death. J Exp Med 182(3):821-8 |
| abstractText | The effect of Bcl-xL upon the developmental death of T cells was assessed by generating transgenic mice that expressed Bcl-xL within all thymocyte subsets. Bcl-xL protected thymocytes from a variety of apoptotic stimuli, including gamma irradiation, glucocorticoids, and anti-CD3 treatment. Bcl-xL altered thymocyte maturation, resulting in increased numbers of CD3int/hi and CD4-8+ thymocytes. Overall, the phenotype of Bcl-xL transgenics was essentially indistinguishable from a Bcl-2 transgenic model. Overexpression of Bcl-xL or Bcl-2 resulted in the down-regulation of the other molecule, providing further evidence of their reciprocal regulation. In a genetic test of redundancy, the Bcl-xL transgene rescued mature T cells in Bcl-2 null mice. Immunoprecipitation indicated that Bcl-xL, like Bcl-2, heterodimerized with the death-promoting molecule Bax in thymocytes. This in vivo model argues that Bcl-xL, like Bcl-2, functions in a common pathway to repress cell death. |
