Bax deficiency partially corrects interleukin-7 receptor α deficiency
Bax deficiency partially corrects interleukin-7 receptor α deficiency
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DOI：
10.1016/s1074-7613(02)00450-8
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发表时间：
2002-11-01
期刊：
影响因子：
32.4
通讯作者：
Durum, SK
中科院分区：
文献类型：
--
作者：
Khaled, AR;Li, WQ;Durum, SK
造血对细胞因子的需求部分归因于保护细胞免于凋亡。由于IL-7是正常T细胞发育所必需的，我们通过产生Bax和IL-7受体α链（IL-7 R）缺陷的小鼠来评估Bax在体内的作用。从出生开始，我们观察到完全恢复的所有阶段的β胸腺细胞发展到4周龄。然而，到12周龄时，胸腺细胞结构已恢复到单独缺乏IL-7 R的小鼠的状态。仅BH 3蛋白质Bad和Bim也是被IL-7抑制的死亡途径的一部分。因此，在幼龄小鼠中，Bax作为由IL-7缺乏诱导的死亡途径中的必需蛋白出现。
The requirement for cytokines in hematopoiesis is partly attributable to the protection of cells from apoptosis. Since IL-7 is required for normal T cell development, we evaluated the role of Bax in vivo by generating mice deficient in both Bax and the IL-7 receptor a chain (IL-7R). Starting at birth, we observed complete recovery of all stages of (3 thymocyte development up to 4 weeks of age. However, by 12 weeks of age, thymic cellularity had reverted to that of mice deficient in IL-7R alone. The BH3 only proteins, Bad and Bim, were also part of the death pathway repressed by IL-7. Thus, in young mice, Bax emerges as an essential protein in the death pathway induced by IL-7 deficiency.