期刊
BIOLOGY OF THE CELL
卷 104, 期 5, 页码 259-270出版社
WILEY-BLACKWELL
DOI: 10.1111/boc.201100055
关键词
Apoptosis; Endoplasmic reticulum; Unfolded protein response
类别
资金
- Science Foundation Ireland [09/RFP/BIC2371, 09/RFP/BMT2153]
- Health Research Board [HRA/2009/59]
- Breast Cancer Campaign [2010NovPR13, 2008NovPhD21]
- European FP6 Apop-Train [MRTN-CT-035624]
- European FP7 EC RTD Integrated Project, Apo-Sys [FP7-200767]
- European Euregional PACT II
- Belgian Interuniversity Attraction Poles [IAP 6/18]
- Flemish Research Foundation Flanders [FWO G.0875.11, FWO G.0973.11]
- Ghent University (MRP, GROUP-ID consortium)
- Flanders Institute for Biotechnology (VIB)
- Flemish Government [BOF09/01M00709]
- FWO
- Health Research Board (HRB) [HRA-2009-59] Funding Source: Health Research Board (HRB)
One of the early cellular responses to endoplasmic reticulum (ER) stress is the activation of the unfolded protein response (UPR). ER stress and the UPR are both implicated in numerous human diseases and pathologies. In spite of this, our knowledge of the molecular mechanisms that regulate cell fate following ER stress is limited. The UPR is initiated by three ER transmembrane receptors: PKR-like ER kinase (PERK), activating transcription factor (ATF) 6 and inositol-requiring enzyme 1 (IRE1). These proteins sense the accumulation of unfolded proteins and their activation triggers specific adaptive responses to resolve the stress. Intriguingly, the very same receptors can initiate signalling pathways that lead to apoptosis when the attempts to resolve the ER stress fail. In this review, we describe the known pro-apoptotic signalling pathways emanating from activated PERK, ATF6 and IRE1 and discuss how their signalling switches from an adaptive to a pro-apoptotic response.
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