Signaling pathways and effector mechanisms pre-programmed cell death

被引：95

作者：

Blatt, NB

Glick, GD ^{[1
]}

机构：

[1] Univ Michigan, Dept Chem, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Dept Biol Chem, Ann Arbor, MI 48109 USA

来源：

BIOORGANIC & MEDICINAL CHEMISTRY | 2001年 / 9卷 / 06期

基金：

美国国家科学基金会; 新加坡国家研究基金会; 美国国家卫生研究院;

关键词：

D O I：

10.1016/S0968-0896(01)00041-4

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 complex biochemical process that involves all aspects of the cell from the plasma membrane to the nucleus. Apoptosis stimuli are mediated by many different cellular processes including protein synthesis and degradation, the alteration in protein phosphorylation states, the activation of lipid second messenger systems, and disruption of normal mitochondrial function. Despite this diversity in signal transduction, all apoptotic pathways are believed to converge ultimately with the activation of caspases leading to the characteristic morphological changes of apoptosis. In this review, we discuss what is known about these pathways and its implication for normal cellular function. (C) 2001 Elsevier Science Ltd. All rights reserved.

引用

收藏

页码：1371 / 1384

页数：14

相关论文

共 157 条

[11] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].

Boldin, MP ;

Goncharov, TM ;

Goltsev, YV ;

Wallach, D .

CELL, 1996, 85 (06) :803-815

[12] Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization [J].

Bossy-Wetzel, E ;

Newmeyer, DD ;

Green, DR .

EMBO JOURNAL, 1998, 17 (01) :37-49

[13] Appearance of phosphatidylserine on apoptotic cells requires calcium-mediated nonspecific flip-flop and is enhanced by loss of the aminophospholipid translocase [J].

Bratton, DL ;

Fadok, VA ;

Richter, DA ;

Kailey, JM ;

Guthrie, LA ;

Henson, PM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (42) :26159-26165

[14] Fas- or ceramide-induced apoptosis is mediated by a rad-regulated activation of jun N-terminal kinase p38 kinases and GADD153 [J].

Brenner, B ;

Koppenhoefer, U ;

Weinstock, C ;

Linderkamp, O ;

Lang, F ;

Gulbins, E .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (35) :22173-22181

[15]

Cahill MA, 1996, ONCOGENE, V13, P2087

[16] Regulation of cell death protease caspase-9 by phosphorylation [J].

Cardone, MH ;

Roy, N ;

Stennicke, HR ;

Salvesen, GS ;

Franke, TF ;

Stanbridge, E ;

Frisch, S ;

Reed, JC .

SCIENCE, 1998, 282 (5392) :1318-1321

[17] Apopain/CPP32 cleaves proteins that are essential for cellular repair: A fundamental principle of apoptotic death [J].

CasciolaRosen, L ;

Nicholson, DW ;

Chong, T ;

Rowan, KR ;

Thornberry, NA ;

Miller, DK ;

Rosen, A .

JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (05) :1957-1964

[18]

CASCIOLAROSEN LA, 1994, J BIOL CHEM, V269, P30757

[19] DNA-DEPENDENT PROTEIN-KINASE IS ONE OF A SUBSET OF AUTOANTIGENS SPECIFICALLY CLEAVED EARLY DURING APOPTOSIS [J].

CASCIOLAROSEN, LA ;

ANHALT, GJ ;

ROSEN, A .

JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (06) :1625-1634

[20]

Castedo M, 1996, J IMMUNOL, V157, P512

← 1 2 3 4 5 6 7 8 9 10 →