ER-stress and apoptosis: molecular mechanisms and potential relevance in infection

被引:40
作者
Haecker, Georg [1 ]
机构
[1] Univ Med Ctr Freiburg, Inst Med Microbiol & Hyg, D-79104 Freiburg, Germany
关键词
ER-stress; Apoptosis; Bcl-2; Infection; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; BH3-ONLY PROTEINS; UP-REGULATION; IMMUNE-RESPONSES; SENSITIZES CELLS; ACTIVATES PERK; MOTOR COMPLEX; MYELOMA CELLS; IN-VIVO;
D O I
10.1016/j.micinf.2014.08.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
During ER-stress, one of the responses a cell can choose is apoptosis. Apoptosis generally is a cell's preferred response when other control mechanisms are overwhelmed. We now have a reasonably clear molecular picture what is happening once the apoptotic apparatus has been started. Unclear however are the majority of the upstream pathways that connect other signalling to apoptosis. During ER-stress, confirmed apoptosis-regulating targets are pro- and anti-apoptotic proteins of the Bcl-2-family, whose concerted action induces apoptosis. I will here discuss how mitochondrial apoptosis is triggered, how this is linked to the ER-stress response and in what way this may be relevant during microbial infections. (C) 2014 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:805 / 810
页数:6
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