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Modulation of neurofibromatosis type 1 gene expression during in vitro myoblast differentiation

dc.contributor.authorGutman, D. H.en_US
dc.contributor.authorCole, Jeffrey L.en_US
dc.contributor.authorCollins, Francis S.en_US
dc.date.accessioned2007-04-06T18:41:15Z
dc.date.available2007-04-06T18:41:15Z
dc.date.issued1994-02-15en_US
dc.identifier.citationGutman, D. H.; Cole, J. L.; Collins, F. S. (1994)."Modulation of neurofibromatosis type 1 gene expression during in vitro myoblast differentiation." Journal of Neuroscience Research 37(3): 398-405. <http://hdl.handle.net/2027.42/50229>en_US
dc.identifier.issn0360-4012en_US
dc.identifier.issn1097-4547en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50229
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8176761&dopt=citationen_US
dc.description.abstractNeurofibromin, the protein product of the neurofibromatiosis type 1 (NF1) gene, has two alternate isoforms which are generated by alternative splicing of two exons. One of these isoforms containing exon 48a is expressed at highest levels in muscle. Since neurofibromin is a p21-ras regulator and has been recently shown to be modulated during Schwann cell differentiation, we examined the expression of the NF1 gene product during in vitro muscle differentiation. Previous work demonstrated that C 2 © 1994 Wiley-Liss, Inc. C 12 murine myoblast cell differentiation could be blocked by the introduction of an activated p21-ras protein. Using this model system, we demonstrate that differentiationg C 2 C 12 cells upregulate the expression of NF1 mRNA by 2 days of serum starvation concomitant with increased expression of nicotinic acetylcholine receptor mRNA. This upregulation of mRNA expression paralleled an increase in neurofibromin and N-ras levels, but no change in the relative abundance of the isoforms containing exon 23a or exon 48a was observed during in vitro myoblast differentiation. The increase in neurofibromin levels paralleled a decrease in the levels of activated p21-ras as assayed by in vivo 32 Porthophosphate incorporation into p21-ras. These results suggest that in vitro C 2 C 12 cell differentiation is associated with a concomitant increase in NF1 gene expression and decrease in the proportion of activated p21-ras. © 1994 Wiley-Liss, Inc.en_US
dc.format.extent900872 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleModulation of neurofibromatosis type 1 gene expression during in vitro myoblast differentiationen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartments of Neurology, Human Genetics, and Internal Medicine and The Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor ; Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St. Louis, MO 63110en_US
dc.contributor.affiliationumDepartments of Neurology, Human Genetics, and Internal Medicine and The Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arboren_US
dc.contributor.affiliationumDepartments of Neurology, Human Genetics, and Internal Medicine and The Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor ; National Center for Human Genome Research, National Institutes of Health, Bethesda, Marylanden_US
dc.identifier.pmid8176761en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50229/1/490370312_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/jnr.490370312en_US
dc.identifier.sourceJournal of Neuroscience Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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