Bcl-XL and Bcl-2 repress a common pathway of cell death.
Bcl-XL and Bcl-2 repress a common pathway of cell death.
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DOI：
10.1084/jem.182.3.821
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发表时间：
1995-09-01
期刊：
影响因子：
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通讯作者：
Korsmeyer SJ
中科院分区：
文献类型：
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作者：
Chao DT;Linette GP;Boise LH;White LS;Thompson CB;Korsmeyer SJ
通过产生在所有胸腺细胞亚群内表达Bcl-xL的转基因小鼠来评估Bcl-xL对T细胞发育性死亡的影响。Bcl-xL保护胸腺细胞免受各种凋亡刺激，包括γ射线照射，糖皮质激素和抗CD 3治疗。Bcl-xL改变胸腺细胞成熟，导致CD 3 int/hi和CD 4 -8+胸腺细胞数量增加。总的来说，Bcl-xL转基因的表型与Bcl-2转基因模型基本上没有区别。Bcl-xL或Bcl-2的过表达导致另一种分子的下调，进一步证明了它们的相互调节。在冗余的遗传测试中，Bcl-xL转基因挽救了Bcl-2缺失小鼠中的成熟T细胞。免疫沉淀表明，Bcl-xL，像Bcl-2，异源二聚体与死亡促进分子Bax在胸腺细胞。这种体内模型认为，Bcl-xL与Bcl-2一样，在抑制细胞死亡的共同途径中发挥作用。
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.