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dc.contributor.authorParkinson, DB
dc.contributor.authorBhaskaran, A
dc.contributor.authorArthur-Farraj, P
dc.contributor.authorNoon, LA
dc.contributor.authorWoodhoo, A
dc.contributor.authorLloyd, AC
dc.contributor.authorFeltri, ML
dc.contributor.authorWrabetz, L
dc.contributor.authorBehrens, A
dc.contributor.authorMirsky, R
dc.contributor.authorJessen, KR
dc.date.accessioned2017-01-03T15:18:18Z
dc.date.available2017-01-03T15:18:18Z
dc.date.issued2008-05-19
dc.identifier.issn0021-9525
dc.identifier.issn1540-8140
dc.identifier.urihttp://hdl.handle.net/10026.1/8174
dc.description.abstract

<jats:p>Schwann cell myelination depends on Krox-20/Egr2 and other promyelin transcription factors that are activated by axonal signals and control the generation of myelin-forming cells. Myelin-forming cells remain remarkably plastic and can revert to the immature phenotype, a process which is seen in injured nerves and demyelinating neuropathies. We report that c-Jun is an important regulator of this plasticity. At physiological levels, c-Jun inhibits myelin gene activation by Krox-20 or cyclic adenosine monophosphate. c-Jun also drives myelinating cells back to the immature state in transected nerves in vivo. Enforced c-Jun expression inhibits myelination in cocultures. Furthermore, c-Jun and Krox-20 show a cross-antagonistic functional relationship. c-Jun therefore negatively regulates the myelinating Schwann cell phenotype, representing a signal that functionally stands in opposition to the promyelin transcription factors. Negative regulation of myelination is likely to have significant implications for three areas of Schwann cell biology: the molecular analysis of plasticity, demyelinating pathologies, and the response of peripheral nerves to injury.</jats:p>

dc.format.extent625-637
dc.format.mediumPrint
dc.languageen
dc.language.isoeng
dc.publisherRockefeller University Press
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectCell Dedifferentiation
dc.subjectCoculture Techniques
dc.subjectCyclic AMP
dc.subjectDNA-Binding Proteins
dc.subjectDown-Regulation
dc.subjectEarly Growth Response Protein 2
dc.subjectGanglia, Spinal
dc.subjectHMGB Proteins
dc.subjectMAP Kinase Kinase 7
dc.subjectMice
dc.subjectMyelin Proteins
dc.subjectMyelin Sheath
dc.subjectOctamer Transcription Factor-6
dc.subjectPhosphorylation
dc.subjectProto-Oncogene Proteins c-jun
dc.subjectRats
dc.subjectSOXB1 Transcription Factors
dc.subjectSchwann Cells
dc.subjectTranscription Factors
dc.subjectUp-Regulation
dc.subjectWallerian Degeneration
dc.titlec-Jun is a negative regulator of myelination
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/18490512
plymouth.issue4
plymouth.volume181
plymouth.publisher-urlhttp://dx.doi.org/10.1083/jcb.200803013
plymouth.publication-statusPublished
plymouth.journalThe Journal of Cell Biology
dc.identifier.doi10.1083/jcb.200803013
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
plymouth.organisational-group/Plymouth/Users by role/Researchers in ResearchFish submission
dc.publisher.placeUnited States
dc.identifier.eissn1540-8140
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1083/jcb.200803013
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review


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