PREVENTION OF PROGRAMMED CELL-DEATH OF SYMPATHETIC NEURONS BY THE BCL-2 PROTOONCOGENE
PREVENTION OF PROGRAMMED CELL-DEATH OF SYMPATHETIC NEURONS BY THE BCL-2 PROTOONCOGENE
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DOI：
10.1126/science.1411528
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发表时间：
1992-10-09
期刊：
影响因子：
56.9
通讯作者：
MARTINOU, JC
中科院分区：
文献类型：
--
作者：
GARCIA, I;MARTINOU, I;MARTINOU, JC
在胚胎发育过程中产生的神经元中，大约有一半通常在成年前死亡。虽然靶源性神经营养因子是程序性细胞死亡-凋亡的主要决定因素，但营养因子干扰细胞死亡调节的分子机制在很大程度上是未知的。在培养的交感神经元中bcl-2原癌基因的过表达现在已被证明可以防止通常由神经生长因子剥夺诱导的细胞凋亡。这一发现，加上以前的演示bcl-2在神经系统中的表达，表明Bcl-2蛋白可能是神经营养因子对神经元存活的影响的主要介质。
Approximately half of the neurons produced during embryogenesis normally die before adulthood. Although target-derived neurotrophic factors are known to be major determinants of programmed cell death-apoptosis-the molecular mechanisms by which trophic factors interfere with cell death regulation are largely unknown. Overexpression of the bcl-2 proto-oncogene in cultured sympathetic neurons has now been shown to prevent apoptosis normally induced by deprivation of nerve growth factor. This finding, together with the previous demonstration of bcl-2 expression in the nervous system, suggests that the Bcl-2 protein may be a major mediator of the effects of neurotrophic factors on neuronal survival.