The UPRER: Sensor and Coordinator of Organismal Homeostasis

被引：258

作者：

Frakes, Ashley E. ^{[1
,2
,3
]}

Dillin, Andrew ^{[1
,2
,3
]}

机构：

[1] Univ Calif Berkeley, Dept Mol & Cell Biol, 229 Stanley Hall, Berkeley, CA 94720 USA

[2] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA

[3] Univ Calif Berkeley, Glenn Ctr Aging Res, Berkeley, CA 94720 USA

来源：

MOLECULAR CELL | 2017年 / 66卷 / 06期

关键词：

UNFOLDED-PROTEIN-RESPONSE; ENDOPLASMIC-RETICULUM STRESS; NF-KAPPA-B; AMYOTROPHIC-LATERAL-SCLEROSIS; TRANSCRIPTION FACTOR XBP-1; INDUCED INSULIN-RESISTANCE; DIPEPTIDE-REPEAT PROTEINS; PLASMA-CELL DIFFERENTIATION; WOLCOTT-RALLISON-SYNDROME; SELECTIVE ER STRESS;

D O I：

10.1016/j.molcel.2017.05.031

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：

Life is stressful. Organisms are repeatedly exposed to stressors that disrupt protein homeostasis (proteostasis), resulting in protein misfolding and aggregation. To sense and respond to proteotoxic perturbations, cells have evolved compartment-specific stress responses, such as the unfolded protein response of the endoplasmic reticulum (UPRER). However, UPRER function is impaired with age, which, we propose, creates a permissive environment for protein aggregation, unresolved ER stress, and chronic inflammation. Understanding age-related changes to the UPRER will provide new avenues for therapeutic intervention in metabolic disease, neurodegeneration, and aging.

引用

收藏

页码：761 / 771

页数：11

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