Show simple item record

dc.contributor.authorLamb, Jennifer A.
dc.contributor.authorVentura, Juan-Jose
dc.contributor.authorHess, Patricia M.
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:09:00.000
dc.date.accessioned2022-08-23T16:14:57Z
dc.date.available2022-08-23T16:14:57Z
dc.date.issued2003-06-25
dc.date.submitted2008-10-15
dc.identifier.citation<p>Mol Cell. 2003 Jun;11(6):1479-89.</p>
dc.identifier.issn1097-2765 (Print)
dc.identifier.doi10.1016/S1097-2765(03)00203-X
dc.identifier.pmid12820962
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33986
dc.description.abstractThe c-Jun NH(2)-terminal kinase (JNK) can cause cell death by activating the mitochondrial apoptosis pathway. However, JNK is also capable of signaling cell survival. The mechanism that accounts for the dual role of JNK in apoptosis and survival signaling has not been established. Here we demonstrate that JNK-stimulated survival signaling can be mediated by JunD. The JNK/JunD pathway can collaborate with NF-kappaB to increase antiapoptotic gene expression. This observation accounts for the ability of JNK to cause either survival or apoptosis in different cellular contexts. Furthermore, these data illustrate the general principal that signal transduction pathway integration is critical for the ability of cells to mount an appropriate biological response to a specific challenge.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12820962&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S1097-2765(03)00203-X
dc.subjectAnimals; Apoptosis; Cell Line; Cell Survival; DNA Fragmentation; Enzyme Activation; Fibroblasts; Gene Expression Regulation; Genes, Reporter; Mice; Mitogen-Activated Protein Kinases; Models, Biological; NF-kappa B; Protein Isoforms; Proto-Oncogene Proteins c-jun; *Signal Transduction; Time Factors; Transcription, Genetic; Tumor Necrosis Factor-alpha
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleJunD mediates survival signaling by the JNK signal transduction pathway
dc.typeJournal Article
dc.source.journaltitleMolecular cell
dc.source.volume11
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/639
dc.identifier.contextkey651109
html.description.abstract<p>The c-Jun NH(2)-terminal kinase (JNK) can cause cell death by activating the mitochondrial apoptosis pathway. However, JNK is also capable of signaling cell survival. The mechanism that accounts for the dual role of JNK in apoptosis and survival signaling has not been established. Here we demonstrate that JNK-stimulated survival signaling can be mediated by JunD. The JNK/JunD pathway can collaborate with NF-kappaB to increase antiapoptotic gene expression. This observation accounts for the ability of JNK to cause either survival or apoptosis in different cellular contexts. Furthermore, these data illustrate the general principal that signal transduction pathway integration is critical for the ability of cells to mount an appropriate biological response to a specific challenge.</p>
dc.identifier.submissionpathgsbs_sp/639
dc.contributor.departmentHoward Hughes Medical Institute and Program in Molecular Medicine
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages1479-89


Files in this item

Thumbnail
Name:
Publisher version

This item appears in the following Collection(s)

Show simple item record