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Requirement of the JIP1 scaffold protein for stress-induced JNK activation

dc.contributor.authorWhitmarsh, Alan J.
dc.contributor.authorKuan, Chia-Yi
dc.contributor.authorKennedy, Norman J.
dc.contributor.authorKelkar, Nyaya
dc.contributor.authorHaydar, Tarik F.
dc.contributor.authorMordes, John P.
dc.contributor.authorAppel, Michael C.
dc.contributor.authorRossini, Aldo A.
dc.contributor.authorJones, Stephen N.
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorRakic, Pasko
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:10:03.000
dc.date.accessioned2022-08-23T16:53:13Z
dc.date.available2022-08-23T16:53:13Z
dc.date.issued2001-09-20
dc.date.submitted2008-07-15
dc.identifier.citation<p>Genes Dev. 2001 Sep 15;15(18):2421-32. <a href="http://dx.doi.org/10.1101/gad.922801">Link to article on publisher's site</a></p>
dc.identifier.issn0890-9369 (Print)
dc.identifier.doi10.1101/gad.922801
dc.identifier.pmid11562351
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42222
dc.description.abstractThe c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=11562351&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC312784/
dc.subject*Adaptor Proteins, Signal Transducing
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectCarrier Proteins
dc.subjectEnzyme Activation
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMitogen-Activated Protein Kinases
dc.subjectNeurons
dc.subject*Oxidative Stress
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleRequirement of the JIP1 scaffold protein for stress-induced JNK activation
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume15
dc.source.issue18
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/589
dc.identifier.contextkey549018
html.description.abstract<p>The c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.</p>
dc.identifier.submissionpathoapubs/589
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentDepartment of Medicine, Division of Diabetes
dc.contributor.departmentDepartment of Cancer Biology
dc.contributor.departmentHoward Hughes Medical Institute and Program in Molecular Medicine
dc.source.pages2421-32


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