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dc.contributor.authorMorel, Caroline
dc.contributor.authorStanden, Claire L.
dc.contributor.authorJung, Dae Young
dc.contributor.authorGray, Susan
dc.contributor.authorOng, Helena
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorKim, Jason K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:16.000
dc.date.accessioned2022-08-23T15:48:50Z
dc.date.available2022-08-23T15:48:50Z
dc.date.issued2010-10-01
dc.date.submitted2016-02-29
dc.identifier.citationMol Cell Biol. 2010 Oct;30(19):4616-25. doi: 10.1128/MCB.00585-10. Epub 2010 Aug 2. <a href="http://dx.doi.org/10.1128/MCB.00585-10">Link to article on publisher's site</a>
dc.identifier.issn0270-7306 (Linking)
dc.identifier.doi10.1128/MCB.00585-10
dc.identifier.pmid20679483
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28296
dc.description.abstractThe c-Jun NH(2)-terminal kinase (JNK) interacting protein 1 (JIP1) has been proposed to act as a scaffold protein that mediates JNK activation. However, recent studies have implicated JIP1 in multiple biochemical processes. Physiological roles of JIP1 that are related to the JNK scaffold function of JIP1 are therefore unclear. To test the role of JIP1 in JNK activation, we created mice with a germ line point mutation in the Jip1 gene (Thr(103) replaced with Ala) that selectively blocks JIP1-mediated JNK activation. These mutant mice exhibit a severe defect in JNK activation caused by feeding of a high-fat diet. The loss of JIP1-mediated JNK activation protected the mutant mice against obesity-induced insulin resistance. We conclude that JIP1-mediated JNK activation plays a critical role in metabolic stress regulation of the JNK signaling pathway.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20679483&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Publisher's PDF posted as allowed by the publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml.</p>
dc.subjectAdaptor Proteins, Signal Transducing
dc.subjectAdipokines
dc.subjectAnimals
dc.subjectBlood Glucose
dc.subjectCytokines
dc.subjectDietary Fats
dc.subjectEnergy Metabolism
dc.subjectEnzyme Activation
dc.subjectFatty Liver
dc.subjectFemale
dc.subjectImmunoblotting
dc.subjectInsulin
dc.subject*Insulin Resistance
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectObesity
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectSignal Transduction
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleRequirement of JIP1-mediated c-Jun N-terminal kinase activation for obesity-induced insulin resistance
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular biology
dc.source.volume30
dc.source.issue19
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1025&amp;context=davis&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/26
dc.identifier.contextkey8234479
refterms.dateFOA2022-08-23T15:48:50Z
html.description.abstract<p>The c-Jun NH(2)-terminal kinase (JNK) interacting protein 1 (JIP1) has been proposed to act as a scaffold protein that mediates JNK activation. However, recent studies have implicated JIP1 in multiple biochemical processes. Physiological roles of JIP1 that are related to the JNK scaffold function of JIP1 are therefore unclear. To test the role of JIP1 in JNK activation, we created mice with a germ line point mutation in the Jip1 gene (Thr(103) replaced with Ala) that selectively blocks JIP1-mediated JNK activation. These mutant mice exhibit a severe defect in JNK activation caused by feeding of a high-fat diet. The loss of JIP1-mediated JNK activation protected the mutant mice against obesity-induced insulin resistance. We conclude that JIP1-mediated JNK activation plays a critical role in metabolic stress regulation of the JNK signaling pathway.</p>
dc.identifier.submissionpathdavis/26
dc.contributor.departmentDepartment of Medicine, Division of Endocrinology, Metabolism and Diabetes
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages4616-25


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