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dc.contributor.authorHotamisligil, Gokhan S.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:19.000
dc.date.accessioned2022-08-23T15:51:04Z
dc.date.available2022-08-23T15:51:04Z
dc.date.issued2016-10-03
dc.date.submitted2016-12-06
dc.identifier.citationCold Spring Harb Perspect Biol. 2016 Oct 3;8(10). pii: a006072. doi: 10.1101/cshperspect.a006072. <a href="http://dx.doi.org/10.1101/cshperspect.a006072">Link to article on publisher's site</a>
dc.identifier.issn1943-0264 (Linking)
dc.identifier.doi10.1101/cshperspect.a006072
dc.identifier.pmid27698029
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28808
dc.description.abstractStress-signaling pathways are evolutionarily conserved and play an important role in the maintenance of homeostasis. These pathways are also critical for adaptation to new cellular environments. The endoplasmic reticulum (ER) unfolded protein response (UPR) is activated by biosynthetic stress and leads to a compensatory increase in ER function. The JNK and p38 MAPK signaling pathways control adaptive responses to intracellular and extracellular stresses, including environmental changes such as UV light, heat, and hyperosmotic conditions, and exposure to inflammatory cytokines. Metabolic stress caused by a high-fat diet represents an example of a stimulus that coordinately activates both the UPR and JNK/p38 signaling pathways. Chronic activation of these stress-response pathways ultimately causes metabolic changes associated with obesity and altered insulin sensitivity. Stress-signaling pathways, therefore, represent potential targets for therapeutic intervention in the metabolic stress response and other disease processes.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27698029&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1101/cshperspect.a006072
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleCell Signaling and Stress Responses
dc.typeJournal Article
dc.source.journaltitleCold Spring Harbor perspectives in biology
dc.source.volume8
dc.source.issue10
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1047
dc.identifier.contextkey9445260
html.description.abstract<p>Stress-signaling pathways are evolutionarily conserved and play an important role in the maintenance of homeostasis. These pathways are also critical for adaptation to new cellular environments. The endoplasmic reticulum (ER) unfolded protein response (UPR) is activated by biosynthetic stress and leads to a compensatory increase in ER function. The JNK and p38 MAPK signaling pathways control adaptive responses to intracellular and extracellular stresses, including environmental changes such as UV light, heat, and hyperosmotic conditions, and exposure to inflammatory cytokines. Metabolic stress caused by a high-fat diet represents an example of a stimulus that coordinately activates both the UPR and JNK/p38 signaling pathways. Chronic activation of these stress-response pathways ultimately causes metabolic changes associated with obesity and altered insulin sensitivity. Stress-signaling pathways, therefore, represent potential targets for therapeutic intervention in the metabolic stress response and other disease processes.</p>
dc.identifier.submissionpathfaculty_pubs/1047
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentProgram in Molecular Medicine


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