PREVENTION OF HYPOXIA-INDUCED CELL-DEATH BY BCL-2 AND BCL-XL

被引：608

作者：

SHIMIZU, S

EGUCHI, Y

KOSAKA, H

KAMIIKE, W

MATSUDA, H

TSUJIMOTO, Y

机构：

[1] OSAKA UNIV,SCH MED,BIOMED RES CTR,DEPT MED GENET,SUITA,OSAKA 565,JAPAN

[2] OSAKA UNIV,SCH MED,DEPT SURG,SUITA,OSAKA 565,JAPAN

[3] OSAKA UNIV,SCH MED,DEPT PHYSIOL,SUITA,OSAKA 565,JAPAN

来源：

NATURE | 1995年 / 374卷 / 6525期

关键词：

D O I：

10.1038/374811a0

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 proto-oncogene bcl-2, isolated from the t(14;18) chromosomal breakpoint in follicular B-lymphoma(1-3), and a bcl-2related gene bcl-x (ref. 4) prevent apoptotic cell death induced by various treatments(5-8). Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS)(910) expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia), which drastically decreases the net formation of oxygen free radicals and does not increase oxidized lipid, protein or DNA. Furthermore, neither ROS scavenger nor inhibitor of ROS scavenger affects cell death, regardless of the expression of Bcl-2 or Bcl-xL. Thus our data suggest that Bcl-2 and Bcl-xL exert an anti-fell death function by a mechanism other than regulation of ROS activity.

引用

页码：811 / 813

页数：3

共 28 条

[1] CLONING THE CHROMOSOMAL BREAKPOINT OF T(14-18) HUMAN LYMPHOMAS - CLUSTERING AROUND JH ON CHROMOSOME-14 AND NEAR A TRANSCRIPTIONAL UNIT ON 18 [J].