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dc.contributor.authorKelkar, Nyaya
dc.contributor.authorGupta, Shashi
dc.contributor.authorDickens, Martin
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:09:33.000
dc.date.accessioned2022-08-23T16:35:30Z
dc.date.available2022-08-23T16:35:30Z
dc.date.issued2000-01-11
dc.date.submitted2009-03-24
dc.identifier.citationMol Cell Biol. 2000 Feb;20(3):1030-43.
dc.identifier.issn0270-7306 (Print)
dc.identifier.pmid10629060
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38572
dc.description.abstractThe c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) is activated in response to the treatment of cells with inflammatory cytokines and by exposure to environmental stress. JNK activation is mediated by a protein kinase cascade composed of a MAPK kinase and a MAPK kinase kinase. Here we describe the molecular cloning of a putative molecular scaffold protein, JIP3, that binds the protein kinase components of a JNK signaling module and facilitates JNK activation in cultured cells. JIP3 is expressed in the brain and at lower levels in the heart and other tissues. Immunofluorescence analysis demonstrated that JIP3 was present in the cytoplasm and accumulated in the growth cones of developing neurites. JIP3 is a member of a novel class of putative MAPK scaffold proteins that may regulate signal transduction by the JNK pathway.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10629060&dopt=Abstract">Link to Article in PubMed</a>
dc.subject*Adaptor Proteins, Signal Transducing
dc.subjectAging
dc.subjectAmino Acid Sequence
dc.subjectAnimals
dc.subjectBrain
dc.subjectCells, Cultured
dc.subjectCloning, Molecular
dc.subjectEmbryonic and Fetal Development
dc.subjectEnzyme Activation
dc.subjectFemale
dc.subject*Gene Expression Regulation, Developmental
dc.subjectGene Library
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMAP Kinase Kinase Kinases
dc.subjectMale
dc.subjectMice
dc.subjectMitogen-Activated Protein Kinases
dc.subjectMolecular Sequence Data
dc.subjectNerve Tissue Proteins
dc.subjectNeurons
dc.subjectProtein Isoforms
dc.subjectRecombinant Proteins
dc.subjectSequence Alignment
dc.subjectSequence Homology, Amino Acid
dc.subjectSignal Transduction
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleInteraction of a mitogen-activated protein kinase signaling module with the neuronal protein JIP3
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular biology
dc.source.volume20
dc.source.issue3
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2438&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1439
dc.identifier.contextkey794936
refterms.dateFOA2022-08-23T16:35:30Z
html.description.abstract<p>The c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) is activated in response to the treatment of cells with inflammatory cytokines and by exposure to environmental stress. JNK activation is mediated by a protein kinase cascade composed of a MAPK kinase and a MAPK kinase kinase. Here we describe the molecular cloning of a putative molecular scaffold protein, JIP3, that binds the protein kinase components of a JNK signaling module and facilitates JNK activation in cultured cells. JIP3 is expressed in the brain and at lower levels in the heart and other tissues. Immunofluorescence analysis demonstrated that JIP3 was present in the cytoplasm and accumulated in the growth cones of developing neurites. JIP3 is a member of a novel class of putative MAPK scaffold proteins that may regulate signal transduction by the JNK pathway.</p>
dc.identifier.submissionpathoapubs/1439
dc.contributor.departmentHoward Hughes Medical Institute, Program in Molecular Medicine
dc.source.pages1030-43


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