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Cited by 945

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

Endoplasmic Reticulum Stress Signaling in Disease

Marciniak, Stefan J., Ron, David·2006·Physiological Reviews

Abstract

The extracellular space is an environment hostile to unmodified polypeptides. For this reason, many eukaryotic proteins destined for exposure to this environment through secretion or display at the cell surface require maturation steps within a specialized organelle, the endoplasmic reticulum (ER). A complex homeostatic mechanism, known as the unfolded protein response (UPR), has evolved to link the load of newly synthesized proteins with the capacity of the ER to mature them. It has become apparent that dysfunction of the UPR plays an important role in some human diseases, especially those involving tissues dedicated to extracellular protein synthesis. Diabetes mellitus is an example of such a disease, since the demands for constantly varying levels of insulin synthesis make pancreatic β-cells dependent on efficient UPR signaling. Furthermore, recent discoveries in this field indicate that the importance of the UPR in diabetes is not restricted to the β-cell but is also involved in peripheral insulin resistance. This review addresses aspects of the UPR currently understood to be involved in human disease, including their role in diabetes mellitus, atherosclerosis, and neoplasia.

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Crossref · 10.1152/physrev.00015.2006

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Metadata

Authors
Marciniak, S. J., & Ron, D.
Venue
Physiological Reviews
Published
2006-10
Volume
86
Issue
4
Pages
1133-1149
ISSN
  • 0031-9333 (ISSN-L)
  • 1522-1210
OpenAlex
W2130326770
Cited by
945
References
15
FWCI
3.87
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Endoplasmic Reticulum Stress Signaling in Disease. https://app.cochat.ai/papers/10.1152/physrev.00015.2006
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Marciniak, S. J., & Ron, D. (2006). Endoplasmic Reticulum Stress Signaling in Disease. Physiological Reviews. https://doi.org/10.1152/physrev.00015.2006

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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.