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dc.contributor.authorBarutcu, Seda
dc.contributor.authorGirnius, Nomeda
dc.contributor.authorVernia, Santiago
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:17.000
dc.date.accessioned2022-08-23T15:49:10Z
dc.date.available2022-08-23T15:49:10Z
dc.date.issued2018-06-28
dc.date.submitted2018-06-29
dc.identifier.citation<p>Autophagy. 2018 Jun 28. doi: 10.1080/15548627.2018.1466013. [Epub ahead of print] <a href="https://doi.org/10.1080/15548627.2018.1466013" target="_blank">Link to article on publisher's site</a></p>
dc.identifier.issn1554-8635
dc.identifier.doi10.1080/15548627.2018.1466013
dc.identifier.pmid29950132
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28368
dc.description.abstractAutophagy is required for cellular homeostasis and can determine cell viability in response to stress. It is established that MTOR is a master regulator of starvation-induced macroautophagy/autophagy, but recent studies have also implicated an essential role for the MAPK8/cJun NH2-terminal kinase 1 signal transduction pathway. We found that MAPK8/JNK1 and MAPK9/JNK2 were not required for autophagy caused by starvation or MTOR inhibition in murine fibroblasts and epithelial cells. These data demonstrate that MAPK8/9 has no required role in starvation-induced autophagy. We conclude that the role of MAPK8/9 in autophagy may be context-dependent and more complex than previously considered.
dc.language.isoen_US
dc.relation<p><a href="https://www.ncbi.nlm.nih.gov/pubmed/29950132" target="_blank">Link to article in PubMed</a></p>
dc.rightsAccepted author version. This is an Open Access article. Non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly attributed, cited, and is not altered, transformed, or built upon in any way, is permitted. The moral rights of the named author(s) have been asserted.
dc.subjectepithelial cell
dc.subjectfibroblast
dc.subjecthepatocyte
dc.subjectMAPK8
dc.subjectMAPK9
dc.subjectMTOR
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleRole of the MAPK/cJun NH2-Terminal Kinase signaling pathway in starvation-induced autophagy
dc.typeAccepted Manuscript
dc.source.journaltitleAutophagy
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1091&amp;context=davis&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/92
dc.identifier.contextkey12417043
refterms.dateFOA2022-08-23T15:49:10Z
html.description.abstract<p>Autophagy is required for cellular homeostasis and can determine cell viability in response to stress. It is established that MTOR is a master regulator of starvation-induced macroautophagy/autophagy, but recent studies have also implicated an essential role for the MAPK8/cJun NH2-terminal kinase 1 signal transduction pathway. We found that MAPK8/JNK1 and MAPK9/JNK2 were not required for autophagy caused by starvation or MTOR inhibition in murine fibroblasts and epithelial cells. These data demonstrate that MAPK8/9 has no required role in starvation-induced autophagy. We conclude that the role of MAPK8/9 in autophagy may be context-dependent and more complex than previously considered.</p>
dc.identifier.submissionpathdavis/92
dc.contributor.departmentGraduate School of Biomedical Sciences, Interdisciplinary Graduate Program
dc.contributor.departmentGraduate School of Biomedical Sciences, Cancer Biology Program
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDavis Lab
dc.contributor.departmentProgram in Molecular Medicine


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