PMID:7650488

Citation	Chao, DT, Linette, GP, Boise, LH, White, LS, Thompson, CB and Korsmeyer, SJ (1995) Bcl-XL and Bcl-2 repress a common pathway of cell death. J. Exp. Med. 182:821-8
Abstract	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.
Links	PubMed PMC2192158
Keywords	Animals; Antibodies, Monoclonal/pharmacology; Antigens, CD3/immunology; Apoptosis/physiology; Dexamethasone/pharmacology; Gamma Rays; Genetic Complementation Test; Lymphocyte Specific Protein Tyrosine Kinase p56(lck); Macromolecular Substances; Mice; Mice, Inbred C57BL; Mice, Transgenic; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/metabolism; Proto-Oncogene Proteins/physiology; Proto-Oncogene Proteins c-bcl-2; Recombinant Fusion Proteins/metabolism; T-Lymphocytes/cytology; T-Lymphocytes/drug effects; T-Lymphocytes/metabolism; T-Lymphocytes/radiation effects; bcl-2-Associated X Protein; bcl-X Protein
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.