MASSIVE CELL-DEATH OF IMMATURE HEMATOPOIETIC-CELLS AND NEURONS IN BCL-X-DEFICIENT MICE
MASSIVE CELL-DEATH OF IMMATURE HEMATOPOIETIC-CELLS AND NEURONS IN BCL-X-DEFICIENT MICE
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DOI：
10.1126/science.7878471
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发表时间：
1995-03-10
期刊：
影响因子：
56.9
通讯作者：
LOH, DY
中科院分区：
文献类型：
--
作者：
MOTOYAMA, N;WANG, FP;LOH, DY
bcl-x是bcl-2基因家族的成员，其可以调节程序性细胞死亡。产生缺乏Bcl-x的小鼠。Bcl-x缺陷小鼠在胚胎第13天左右死亡。在发育中的大脑、脊髓和背根神经节的有丝分裂后未成熟神经元中，广泛的凋亡细胞死亡是明显的。肝脏造血细胞也发生凋亡。对bcl-x双敲除嵌合体小鼠的分析表明，Bcl-x缺陷型淋巴细胞的成熟减少。未成熟淋巴细胞的寿命缩短，但成熟淋巴细胞的寿命没有缩短。因此，Bcl-x的功能是在神经和造血系统发育期间支持未成熟细胞的活力。
bcl-x is a member of the bcl-2 gene family, which may regulate programmed cell death. Mice were generated that lacked Bcl-x. The Bcl-x-deficient mice died around embryonic day 13. Extensive apoptotic cell death was evident in postmitotic immature neurons of the developing brain, spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver were also apoptotic. Analyses of bcl-x double-knockout chimeric mice showed that the maturation of Bcl-x-deficient lymphocytes was diminished. The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development oi the nervous and hematopoietic systems.