Modulation of neurofibromatosis type 1 gene expression during in vitro myoblast differentiation
dc.contributor.author | Gutman, D. H. | en_US |
dc.contributor.author | Cole, Jeffrey L. | en_US |
dc.contributor.author | Collins, Francis S. | en_US |
dc.date.accessioned | 2007-04-06T18:41:15Z | |
dc.date.available | 2007-04-06T18:41:15Z | |
dc.date.issued | 1994-02-15 | en_US |
dc.identifier.citation | Gutman, 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.issn | 0360-4012 | en_US |
dc.identifier.issn | 1097-4547 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/50229 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8176761&dopt=citation | en_US |
dc.description.abstract | Neurofibromin, 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.extent | 900872 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | Modulation of neurofibromatosis type 1 gene expression during in vitro myoblast differentiation | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Psychology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Social Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Departments 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 63110 | en_US |
dc.contributor.affiliationum | Departments of Neurology, Human Genetics, and Internal Medicine and The Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor | en_US |
dc.contributor.affiliationum | Departments 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, Maryland | en_US |
dc.identifier.pmid | 8176761 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/50229/1/490370312_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jnr.490370312 | en_US |
dc.identifier.source | Journal of Neuroscience Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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