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dc.contributor.authorKelkar, Nyaya
dc.contributor.authorDelmotte, Marie Helene
dc.contributor.authorWeston, Claire R.
dc.contributor.authorBarrett, Tamera
dc.contributor.authorSheppard, Barbara J.
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:06Z
dc.date.available2022-08-23T16:37:06Z
dc.date.issued2003-08-05
dc.date.submitted2009-04-02
dc.identifier.citation<p>Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9843-8. Epub 2003 Aug 1. <a href="http://dx.doi.org/10.1073/pnas.1733944100">Link to article on publisher's site</a></p>
dc.identifier.issn0027-8424 (Print)
dc.identifier.doi10.1073/pnas.1733944100
dc.identifier.pmid12897243
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38938
dc.description.abstractThe murine JNK-interacting protein 3 (JIP3) protein (also known as JSAP1) is expressed exclusively in neurons and has been identified as a scaffold protein for the c-Jun NH2-terminal kinase (JNK) signaling pathway and as an adapter protein for cargo transport by the microtubule motor protein kinesin. To investigate the physiological function of JIP3, we examined the effect of Jip3 gene disruption in mice. The Jip3-/- mice were unable to breathe and died shortly after birth. Microscopic analysis demonstrated that Jip3 gene disruption causes severe defects in the morphogenesis of the telencephalon. Jip3-/- mice lack the telencephalic commissure, a major connection between the left and right hemispheres of the brain. The central nervous system abnormalities of Jip3-/- mice may be accounted for in part by a reduction in signal transduction by RhoA and its effector ROCK.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12897243&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC187860/
dc.subject*Adaptor Proteins, Signal Transducing
dc.subjectAnimals
dc.subjectGene Expression Regulation, Developmental
dc.subjectGene Targeting
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMitogen-Activated Protein Kinases
dc.subjectMunc18 Proteins
dc.subjectNerve Tissue Proteins
dc.subjectProteins
dc.subjectSignal Transduction
dc.subjectTelencephalon
dc.subject*Vesicular Transport Proteins
dc.subjectrhoA GTP-Binding Protein
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleMorphogenesis of the telencephalic commissure requires scaffold protein JNK-interacting protein 3 (JIP3)
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume100
dc.source.issue17
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1769
dc.identifier.contextkey808534
html.description.abstract<p>The murine JNK-interacting protein 3 (JIP3) protein (also known as JSAP1) is expressed exclusively in neurons and has been identified as a scaffold protein for the c-Jun NH2-terminal kinase (JNK) signaling pathway and as an adapter protein for cargo transport by the microtubule motor protein kinesin. To investigate the physiological function of JIP3, we examined the effect of Jip3 gene disruption in mice. The Jip3-/- mice were unable to breathe and died shortly after birth. Microscopic analysis demonstrated that Jip3 gene disruption causes severe defects in the morphogenesis of the telencephalon. Jip3-/- mice lack the telencephalic commissure, a major connection between the left and right hemispheres of the brain. The central nervous system abnormalities of Jip3-/- mice may be accounted for in part by a reduction in signal transduction by RhoA and its effector ROCK.</p>
dc.identifier.submissionpathoapubs/1769
dc.contributor.departmentHoward Hughes Medical Institute and Program in Molecular Medicine
dc.source.pages9843-8


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