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Cited by 402

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Signaling cell death from the endoplasmic reticulum stress response

Open access
Shore, Gordon C, Papa, Feroz R, Oakes, Scott A·2011·Current Opinion in Cell Biology

Abstract

Summary 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.

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Crossref · 10.1016/j.ceb.2010.11.003

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Metadata

Authors
Shore, G. C., Papa, F. R., & Oakes, S. A.
Venue
Current Opinion in Cell Biology
Publisher
Elsevier BV
Published
2011-04
Volume
23
Issue
2
Pages
143-149
ISSN
0955-0674 (ISSN-L)
OpenAlex
W2162969910
Cited by
402
References
6
FWCI
1.24
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Signaling cell death from the endoplasmic reticulum stress response. https://app.cochat.ai/papers/10.1016/j.ceb.2010.11.003
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Shore, G. C., Papa, F. R., & Oakes, S. A. (2011). Signaling cell death from the endoplasmic reticulum stress response. Current Opinion in Cell Biology. https://doi.org/10.1016/j.ceb.2010.11.003

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.