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dc.contributor.authorVernia, Santiagoen_US
dc.contributor.authorMorel, Carolineen_US
dc.contributor.authorMadara, Joseph Cen_US
dc.contributor.authorCavanagh-Kyros, Julieen_US
dc.contributor.authorBarrett, Tameraen_US
dc.contributor.authorChase, Kathrynen_US
dc.contributor.authorKennedy, Norman Jen_US
dc.contributor.authorJung, Dae Youngen_US
dc.contributor.authorKim, Jason Ken_US
dc.contributor.authorAronin, Neilen_US
dc.contributor.authorFlavell, Richard Aen_US
dc.contributor.authorLowell, Bradford Ben_US
dc.contributor.authorDavis, Roger Jen_US
dc.date.accessioned2016-04-01T15:47:33Z
dc.date.issued2016en_US
dc.identifier.citationVernia, S., C. Morel, J. C. Madara, J. Cavanagh-Kyros, T. Barrett, K. Chase, N. J. Kennedy, et al. 2016. “Excitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stress.” eLife 5 (1): e10031. doi:10.7554/eLife.10031. http://dx.doi.org/10.7554/eLife.10031.en
dc.identifier.issn2050-084Xen
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:26318539
dc.description.abstractThe cJun NH2-terminal kinase (JNK) signaling pathway is implicated in the response to metabolic stress. Indeed, it is established that the ubiquitously expressed JNK1 and JNK2 isoforms regulate energy expenditure and insulin resistance. However, the role of the neuron-specific isoform JNK3 is unclear. Here we demonstrate that JNK3 deficiency causes hyperphagia selectively in high fat diet (HFD)-fed mice. JNK3 deficiency in neurons that express the leptin receptor LEPRb was sufficient to cause HFD-dependent hyperphagia. Studies of sub-groups of leptin-responsive neurons demonstrated that JNK3 deficiency in AgRP neurons, but not POMC neurons, was sufficient to cause the hyperphagic response. These effects of JNK3 deficiency were associated with enhanced excitatory signaling by AgRP neurons in HFD-fed mice. JNK3 therefore provides a mechanism that contributes to homeostatic regulation of energy balance in response to metabolic stress. DOI: http://dx.doi.org/10.7554/eLife.10031.001en
dc.language.isoen_USen
dc.publishereLife Sciences Publications, Ltden
dc.relation.isversionofdoi:10.7554/eLife.10031en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4798947/pdf/en
dash.licenseLAAen_US
dc.subjectsignal transductionen
dc.subjectJNKen
dc.subjectleptinen
dc.subjectsatietyen
dc.subjectMouseen
dc.titleExcitatory transmission onto AgRP neurons is regulated by cJun NH2-terminal kinase 3 in response to metabolic stressen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journaleLifeen
dash.depositing.authorMadara, Joseph Cen_US
dc.date.available2016-04-01T15:47:33Z
dc.identifier.doi10.7554/eLife.10031*
dash.authorsorderedfalse
dash.contributor.affiliatedLowell, Bradford
dash.contributor.affiliatedMadara, Joseph


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