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dc.contributor.authorKant, Shashi
dc.contributor.authorBarrett, Tamera
dc.contributor.authorVertii, Anastassiia
dc.contributor.authorNoh, Yun Hee
dc.contributor.authorJung, Dae Young
dc.contributor.authorKim, Jason K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:10:18.000
dc.date.accessioned2022-08-23T17:03:18Z
dc.date.available2022-08-23T17:03:18Z
dc.date.issued2013-08-29
dc.date.submitted2014-04-14
dc.identifier.citationKant S, Barrett T, Vertii A, Noh YH, Jung DY, Kim JK, Davis RJ. Role of the mixed-lineage protein kinase pathway in the metabolic stress response to obesity. Cell Rep. 2013 Aug 29;4(4):681-8. doi: 10.1016/j.celrep.2013.07.019. <a href="http://dx.doi.org/10.1016/j.celrep.2013.07.019">Link to article on publisher's site</a>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2013.07.019
dc.identifier.pmid23954791
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44395
dc.description.abstractSaturated free fatty acid (FFA) is implicated in the metabolic response to obesity. In vitro studies indicate that FFA signaling may be mediated by the mixed-lineage protein kinase (MLK) pathway that activates cJun NH2-terminal kinase (JNK). Here, we examined the role of the MLK pathway in vivo using a mouse model of diet-induced obesity. The ubiquitously expressed MLK2 and MLK3 protein kinases have partially redundant functions. We therefore compared wild-type and compound mutant mice that lack expression of MLK2 and MLK3. MLK deficiency protected mice against high-fat-diet-induced insulin resistance and obesity. Reduced JNK activation and increased energy expenditure contribute to the metabolic effects of MLK deficiency. These data confirm that the MLK pathway plays a critical role in the metabolic response to obesity.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23954791&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.</p>
dc.subjectAnimals
dc.subjectDiet, High-Fat
dc.subjectInsulin Resistance
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMAP Kinase Kinase Kinases
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMutation
dc.subjectObesity
dc.subject*Stress, Physiological
dc.subjectBiochemistry
dc.subjectCellular and Molecular Physiology
dc.titleRole of the mixed-lineage protein kinase pathway in the metabolic stress response to obesity
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume4
dc.source.issue4
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1012&amp;context=pmm_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/13
dc.identifier.contextkey5476843
refterms.dateFOA2022-08-23T17:03:18Z
html.description.abstract<p>Saturated free fatty acid (FFA) is implicated in the metabolic response to obesity. In vitro studies indicate that FFA signaling may be mediated by the mixed-lineage protein kinase (MLK) pathway that activates cJun NH2-terminal kinase (JNK). Here, we examined the role of the MLK pathway in vivo using a mouse model of diet-induced obesity. The ubiquitously expressed MLK2 and MLK3 protein kinases have partially redundant functions. We therefore compared wild-type and compound mutant mice that lack expression of MLK2 and MLK3. MLK deficiency protected mice against high-fat-diet-induced insulin resistance and obesity. Reduced JNK activation and increased energy expenditure contribute to the metabolic effects of MLK deficiency. These data confirm that the MLK pathway plays a critical role in the metabolic response to obesity.</p>
dc.identifier.submissionpathpmm_pp/13
dc.contributor.departmentDepartment of Medicine, Division of Endocrinology, Metabolism and Diabetes
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages681-8


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