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dc.contributor.authorGirnius, Nomeda A.
dc.contributor.authorEdwards, Yvonne J. K.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:22.000
dc.date.accessioned2022-08-23T15:52:59Z
dc.date.available2022-08-23T15:52:59Z
dc.date.issued2018-03-06
dc.date.submitted2018-04-09
dc.identifier.citation<p>Cell Death Differ. 2018 Mar 6. doi: 10.1038/s41418-018-0081-z. [Epub ahead of print] <a href="https://doi.org/10.1038/s41418-018-0081-z">Link to article on publisher's site</a></p>
dc.identifier.issn1350-9047 (Linking)
dc.identifier.doi10.1038/s41418-018-0081-z
dc.identifier.pmid29511338
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29262
dc.description.abstractInvolution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell compartment. To test whether the cJUN NH2-terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice with JNK deficiency in the mammary epithelium. We found that JNK is required for efficient involution. JNK deficiency did not alter the STAT3/5 or SMAD2/3 signaling pathways that have been previously implicated in this process. Nevertheless, JNK promotes the expression of genes that drive involution, including matrix metalloproteases, cathepsins, and BH3-only proteins. These data demonstrate that JNK has a key role in mammary gland involution post lactation.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29511338&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rights© The Author(s) 2018. This article is published with open access. Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectGene expression
dc.subjectKinases
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectCell and Developmental Biology
dc.subjectCellular and Molecular Physiology
dc.subjectEnzymes and Coenzymes
dc.subjectGenetic Phenomena
dc.titleThe cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution
dc.typeArticle
dc.source.journaltitleCell death and differentiation
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2496&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1493
dc.identifier.contextkey11928422
refterms.dateFOA2022-08-23T15:53:00Z
html.description.abstract<p>Involution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell compartment. To test whether the cJUN NH2-terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice with JNK deficiency in the mammary epithelium. We found that JNK is required for efficient involution. JNK deficiency did not alter the STAT3/5 or SMAD2/3 signaling pathways that have been previously implicated in this process. Nevertheless, JNK promotes the expression of genes that drive involution, including matrix metalloproteases, cathepsins, and BH3-only proteins. These data demonstrate that JNK has a key role in mammary gland involution post lactation.</p>
dc.identifier.submissionpathfaculty_pubs/1493
dc.contributor.departmentDavis Lab
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentProgram in Molecular Medicine


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© The Author(s) 2018. This article is published with open access.  Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Except where otherwise noted, this item's license is described as © The Author(s) 2018. This article is published with open access. Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.