Signaling cell death from the endoplasmic reticulum stress response.

Abstract:

:Inability to meet protein folding demands within the endoplasmic reticulum (ER) activates the unfolded protein response (UPR), a signaling pathway with both adaptive and apoptotic outputs. While some secretory cell types have a remarkable ability to increase protein folding capacity, their upper limits can be reached when pathological conditions overwhelm the fidelity and/or output of the secretory pathway. Irremediable 'ER stress' induces apoptosis and contributes to cell loss in several common human diseases, including type 2 diabetes and neurodegeneration. Researchers have begun to elucidate the molecular switches that determine when ER stress is too great to repair and the signals that are then sent from the UPR to execute the cell.

journal_name

Curr Opin Cell Biol

authors

Shore GC,Papa FR,Oakes SA

doi

10.1016/j.ceb.2010.11.003

subject

Has Abstract

pub_date

2011-04-01 00:00:00

pages

143-9

issue

2

eissn

0955-0674

issn

1879-0410

pii

S0955-0674(10)00209-7

journal_volume

23

pub_type

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