BCL-2 INHIBITS DEATH OF CENTRAL NEURAL CELLS INDUCED BY MULTIPLE AGENTS

被引：617

作者：

ZHONG, LT

SARAFIAN, T

KANE, DJ

CHARLES, AC

MAH, SP

EDWARDS, RH

BREDESEN, DE

机构：

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

[2] UNIV CALIF LOS ANGELES,SCH MED,DEPT PATHOL,LOS ANGELES,CA 90024

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 10期

关键词：

APOPTOSIS; CALCIUM; IMMORTALIZED CELLS; PROGRAMMED CELL DEATH;

D O I：

10.1073/pnas.90.10.4533

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The protooncogene bcl-2, which has been implicated in B-cell lymphoma development, inhibits apoptosis due to growth factor withdrawal in some, but not all, hematopoietic cells. Recently we found that bcl-2 also inhibits apoptosis in PC12 pheochromocytoma cells. We now report that bcl-2 inhibits the death of a central neural cell line due to serum and growth factor withdrawal, the calcium ionophore A23187, glucose withdrawal, membrane peroxidation, and, in some cases, free radical-induced damage. This broad range of protective effects of BCL-2 protein suggests that BCL-2 may interact with a central step in neural cell death. Measurements of intracellular free calcium suggest that BCL-2 alters the transduction of neural death signals at a point distal to the rise in intracellular free calcium.

引用

页码：4533 / 4537

页数：5

共 36 条

[1] OVEREXPRESSED FULL-LENGTH HUMAN BCL2 EXTENDS THE SURVIVAL OF BACULOVIRUS-INFECTED SF9 INSECT CELLS [J].