Bcl-XL and Bcl-2 repress a common pathway of cell death.

DT Chao, GP Linette, LH Boise, LS White… - The Journal of …, 1995 - rupress.org
DT Chao, GP Linette, LH Boise, LS White, CB Thompson, SJ Korsmeyer
The Journal of experimental medicine, 1995rupress.org
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 …
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.
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