A caspase homolog keeps CED-3 in check

被引：7

作者：

Brady, Graham F. ^{[1
]}

Duckett, Colin S. ^{[1
,2
]}

机构：

[1] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2009年 / 34卷 / 03期

基金：

美国国家卫生研究院;

关键词：

MAMMALIAN INTERLEUKIN-1-BETA-CONVERTING ENZYME; PROGRAMMED CELL-DEATH; CAENORHABDITIS-ELEGANS; C-ELEGANS; PROTEIN CED-3; GENE CED-3; APOPTOSIS; INHIBITOR; ACTIVATION; GENERATION;

D O I：

10.1016/j.tibs.2008.11.003

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：

Apoptosis is a highly conserved form of cell death that is essential for controlling cell numbers throughout the lifetime of an organism. In Caenorhabditis elegans, the final step in the apoptotic cascade is activation of the death-inducing protease CED-3. Until now, no direct negative regulators of CED-3 had been identified, so the mechanism for maintaining a proper life-death balance was unclear. Now, a new study identifies CSP-3 as an important negative regulator of CED-3 during C. elegans development.

引用

页码：104 / 107

页数：4

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