Endoplasmic reticulum stress and apoptosis

被引:154
作者
Faitova, Jitka [1 ]
Krekac, Daniel [1 ]
Hrstka, Roman [1 ]
Vojtesek, Borivoj [1 ]
机构
[1] Masaryk Mem Canc Inst, Dept Pathol & Expt Oncol, Brno 65653, Czech Republic
关键词
endoplasmic reticulum; apoptosis; p53; scotin;
D O I
10.2478/s11658-006-0040-4
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
Cell death is an essential event in normal life and development, as well as in the pathophysiological processes that lead to disease. It has become clear that each of the main cellular organelles can participate in cell death signalling pathways, and recent advances have highlighted the importance of the endoplasmic reticulum (ER) in cell death processes. In cells, the ER functions as the organelle where proteins mature, and as such, is very responsive to extracellular-intracellular changes of environment. This short overview focuses on the known pathways of programmed cell death triggering from or involving the ER.
引用
收藏
页码:488 / 505
页数:18
相关论文
共 82 条
[1]   CHOP (GADD153) AND ITS ONCOGENIC VARIANT, TLS-CHOP, HAVE OPPOSING EFFECTS ON THE INDUCTION OF G(1)/S ARREST [J].
BARONE, MV ;
CROZAT, A ;
TABAEE, A ;
PHILIPSON, L ;
RON, D .
GENES & DEVELOPMENT, 1994, 8 (04) :453-464
[2]  
BLONDELGUINDI S, 1993, J BIOL CHEM, V268, P12730
[3]   Further characterisation of the p53 responsive element - Identification of new candidate genes for trans-activation by p53 [J].
Bourdon, JC ;
DeguinChambon, V ;
Lelong, JC ;
Dessen, P ;
May, P ;
Debuire, B ;
May, E .
ONCOGENE, 1997, 14 (01) :85-94
[4]   Endoplasmic reticulum stress-induced cell death requires mitochondrial membrane permeabilization [J].
Boya, P ;
Cohen, I ;
Zamzami, N ;
Vieira, HLA ;
Kroemer, G .
CELL DEATH AND DIFFERENTIATION, 2002, 9 (04) :465-467
[5]   The procaspase-8 isoform, procaspase-8L, recruited to the BAP31 complex at the endoplasmic reticulum [J].
Breckenridge, DG ;
Nguyen, M ;
Kuppig, S ;
Reth, M ;
Shore, GC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (07) :4331-4336
[6]   Regulation of apoptosis by endoplasmic reticulum pathways [J].
Breckenridge, DG ;
Germain, M ;
Mathai, JP ;
Nguyen, M ;
Shore, GC .
ONCOGENE, 2003, 22 (53) :8608-8618
[7]   IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA [J].
Calfon, M ;
Zeng, HQ ;
Urano, F ;
Till, JH ;
Hubbard, SR ;
Harding, HP ;
Clark, SG ;
Ron, D .
NATURE, 2002, 415 (6867) :92-96
[8]   Bcl-2 and Bax exert opposing effects on Ca2+ signaling, which do not depend on their putative pore-forming region [J].
Chami, M ;
Prandini, A ;
Campanella, M ;
Pinton, P ;
Szabadkai, G ;
Reed, JC ;
Rizzuto, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (52) :54581-54589
[9]   Endoplasmic reticulum stress induces apoptosis by an apoptosome-dependent but caspase 12-independent mechanism [J].
Di Sano, F ;
Ferraro, E ;
Tufi, R ;
Achsel, T ;
Piacentini, M ;
Cecconi, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (05) :2693-2700
[10]   Human caspase 12 has acquired deleterious mutations [J].
Fischer, H ;
Koenig, U ;
Eckhart, L ;
Tschachler, E .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 293 (02) :722-726