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dc.contributor.authorSabio, Guadalupe
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:16.000
dc.date.accessioned2022-08-23T15:48:49Z
dc.date.available2022-08-23T15:48:49Z
dc.date.issued2010-09-01
dc.date.submitted2016-02-29
dc.identifier.citationTrends Biochem Sci. 2010 Sep;35(9):490-6. doi: 10.1016/j.tibs.2010.04.004. Epub 2010 May 7. <a href="http://dx.doi.org/10.1016/j.tibs.2010.04.004">Link to article on publisher's site</a>
dc.identifier.issn0968-0004 (Linking)
dc.identifier.doi10.1016/j.tibs.2010.04.004
dc.identifier.pmid20452774
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28293
dc.description.abstractThe cJun NH(2)-terminal kinase isoform JNK1 is implicated in the mechanism of obesity-induced insulin resistance. Feeding a high-fat diet causes activation of the JNK1 signaling pathway, insulin resistance, and obesity in mice. Germ-line ablation of Jnk1 prevents both diet-induced obesity and insulin resistance. Genetic analysis indicates that the effects of JNK1 on insulin resistance can be separated from effects of JNK1 on obesity. Emerging research indicates that JNK1 plays multiple roles in the regulation of insulin resistance, including altered gene expression, hormone/cytokine production, and lipid metabolism. Together, these studies establish JNK1 as a potential pharmacological target for the development of drugs that might be useful for the treatment of insulin resistance, metabolic syndrome, and type 2 diabetes.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20452774&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975251/
dc.subjectAnimals
dc.subjectDiet
dc.subjectHumans
dc.subject*Insulin Resistance
dc.subjectInsulin-Secreting Cells
dc.subjectMice
dc.subjectMitogen-Activated Protein Kinase 8
dc.subjectObesity
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titlecJun NH2-terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance
dc.typeJournal Article
dc.source.journaltitleTrends in biochemical sciences
dc.source.volume35
dc.source.issue9
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/23
dc.identifier.contextkey8234475
html.description.abstract<p>The cJun NH(2)-terminal kinase isoform JNK1 is implicated in the mechanism of obesity-induced insulin resistance. Feeding a high-fat diet causes activation of the JNK1 signaling pathway, insulin resistance, and obesity in mice. Germ-line ablation of Jnk1 prevents both diet-induced obesity and insulin resistance. Genetic analysis indicates that the effects of JNK1 on insulin resistance can be separated from effects of JNK1 on obesity. Emerging research indicates that JNK1 plays multiple roles in the regulation of insulin resistance, including altered gene expression, hormone/cytokine production, and lipid metabolism. Together, these studies establish JNK1 as a potential pharmacological target for the development of drugs that might be useful for the treatment of insulin resistance, metabolic syndrome, and type 2 diabetes.</p>
dc.identifier.submissionpathdavis/23
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages490-6


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