Mechanisms, regulation and functions of the unfolded protein response.


Journal

Nature reviews. Molecular cell biology
ISSN: 1471-0080
Titre abrégé: Nat Rev Mol Cell Biol
Pays: England
ID NLM: 100962782

Informations de publication

Date de publication:
08 2020
Historique:
accepted: 14 04 2020
pubmed: 28 5 2020
medline: 11 11 2020
entrez: 28 5 2020
Statut: ppublish

Résumé

Cellular stress induced by the abnormal accumulation of unfolded or misfolded proteins at the endoplasmic reticulum (ER) is emerging as a possible driver of human diseases, including cancer, diabetes, obesity and neurodegeneration. ER proteostasis surveillance is mediated by the unfolded protein response (UPR), a signal transduction pathway that senses the fidelity of protein folding in the ER lumen. The UPR transmits information about protein folding status to the nucleus and cytosol to adjust the protein folding capacity of the cell or, in the event of chronic damage, induce apoptotic cell death. Recent advances in the understanding of the regulation of UPR signalling and its implications in the pathophysiology of disease might open new therapeutic avenues.

Identifiants

pubmed: 32457508
doi: 10.1038/s41580-020-0250-z
pii: 10.1038/s41580-020-0250-z
pmc: PMC8867924
mid: NIHMS1773650
doi:

Substances chimiques

Proteins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

421-438

Subventions

Organisme : NIDDK NIH HHS
ID : R24 DK110973
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA030199
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK103185
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK113171
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR066634
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA198103
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK063491
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK090313
Pays : United States

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Auteurs

Claudio Hetz (C)

Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile. chetz@med.uchile.cl.
FONDAP Center for Geroscience Brain Health and Metabolism (GERO), Santiago, Chile. chetz@med.uchile.cl.
Program of Cellular and Molecular Biology, Institute of Biomedical Science, University of Chile, Santiago, Chile. chetz@med.uchile.cl.
Buck Institute for Research on Aging, Novato, CA, USA. chetz@med.uchile.cl.

Kezhong Zhang (K)

Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI, USA. kzhang@med.wayne.edu.
Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, MI, USA. kzhang@med.wayne.edu.

Randal J Kaufman (RJ)

Degenerative Diseases Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA. rkaufman@sbpdiscovery.org.

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