THE PROTOONCOGENE BCL-2 INHIBITS APOPTOSIS IN PC12 CELLS

被引：236

作者：

MAH, SP ^{[1
]}

ZHONG, LT ^{[1
]}

LIU, Y ^{[1
]}

ROGHANI, A ^{[1
]}

EDWARDS, RH ^{[1
]}

BREDESEN, DE ^{[1
]}

机构：

[1] UNIV CALIF LOS ANGELES, SCH MED,DEPT NEUROL,REED NEUROL RES CTR, 710 WESTWOOD PLAZA, LOS ANGELES, CA 90024 USA

来源：

JOURNAL OF NEUROCHEMISTRY | 1993年 / 60卷 / 03期

关键词：

APOPTOSIS; BCL-2; NEUROTROPHIC FACTORS; PC12-CELLS;

D O I：

10.1111/j.1471-4159.1993.tb03275.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

During development, many neuronal populations undergo a process of normal, programmed cell death, or apoptosis. Trophic factors regulate this process, but the mechanism by which they suppress apoptosis remains unclear. In the immune system, recent studies have implicated the protooncogene bcl-2 in the lymphocyte survival response to growth factors. To determine whether a similar survival pathway exists in a neuroendocrine cell type, we have expressed bcl-2 in the rat pheochromocytoma PC12 cell line and found that it abrogates the requirement for stimulation by growth factors to survive. bcl-2 expression also substantially delays the onset of injury by the calcium ionophore A23187.

引用

页码：1183 / 1186

页数：4

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