Modulation of the neurofibromatosis type 1 gene product, neurofibromin, during Schwann cell differentiation

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dc.contributor.author Gutmann, D. H. en_US
dc.contributor.author Tennekoon, Gihan I. en_US
dc.contributor.author Cole, Jeffrey L. en_US
dc.contributor.author Collins, Francis S. en_US
dc.contributor.author Rutkowski, J. Lynn en_US
dc.date.accessioned 2007-04-06T18:41:02Z
dc.date.available 2007-04-06T18:41:02Z
dc.date.issued 1993-10-01 en_US
dc.identifier.citation Gutmann, D. H.; Tennekoon, G. I.; Cole, J. L.; Collins, F. S.; Rutkowski, J. L. (1993)."Modulation of the neurofibromatosis type 1 gene product, neurofibromin, during Schwann cell differentiation." Journal of Neuroscience Research 36(2): 216-223. <http://hdl.handle.net/2027.42/50227> en_US
dc.identifier.issn 0360-4012 en_US
dc.identifier.issn 1097-4547 en_US
dc.identifier.uri http://hdl.handle.net/2027.42/50227
dc.identifier.uri http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7505343&dopt=citation en_US
dc.description.abstract Neurofibromin, the product of the neurofibromatosis type 1 (NF1) gene, is a ∼250 kDa protein expressed predominantly in cortical neurons and oligodendrocytes in the central nervous system (CNS) and sensory neurons and Schwann cells in the peripheral nervous system (PNS). To gain insight into the biological role of neurofibromin in Schwann cells, the modulation of NF1 gene expression in a Schwann cell line (MT 4 H1) stimulated to either proliferate or differentiate in response to agents that elevate intracellular cAMP was examined. Untreated cells and cells exposed to mitogenic doses of forskolin (1–10 ΜM) or 8-bromo-cAMP (0.1 mM) expressed low levels of NF1 MRNA and the protein was barely detectable. High doses of forskolin (100 ΜM) or 8-bromo-cAMP (1 mM) induced the expression of both myelin P 0 protein and neurofibromin with an identical time course. Although NF1 mRNA levels peaked within 1–6 hr, the rise in neurofibromin was not apparent until 24–48 hr and peaked 72 hr after treatment. P 0 and neurofibromin were also coinduced by cell-cell contact in high density, untreated cultures. Moreover, differentiation initiated by either cAMP stimulation or high density culture conditions was associated with predominant expression of the type 2 NF1 mRNA isoform. In contrast, type 1 NF1 mRNA isoform expression was observed in untreated Schwann cells or those stimulated with mitogenic doses of forskolin or 8-bromo-cAMP. A switch from the type 1 neurofibromin that can efficiently down-regulate p21-ras to the type 2 isoform with reduced activity may facilitate a p21-ras signaling pathway associated with Schwann cell difrerentiation. © 1993 Wiley-Liss, Inc. en_US
dc.format.extent 822589 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 the neurofibromatosis type 1 gene product, neurofibromin, during Schwann cell 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, University of Michigan Medical Center, Ann Arbor ; Departments of Internal Medicine, University of Michigan Medical Center, Ann Arbor ; Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor ; 4570 MSRB 2, Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI 48109-0650 en_US
dc.contributor.affiliationum Departments of Pediatrics, University of Michigan Medical Center, Ann Arbor en_US
dc.contributor.affiliationum Departments of Internal Medicine, University of Michigan Medical Center, Ann Arbor ; Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor en_US
dc.contributor.affiliationum Departments of Human Genetics, University of Michigan Medical Center, Ann Arbor ; Departments of Internal Medicine, University of Michigan Medical Center, Ann Arbor ; Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor en_US
dc.contributor.affiliationum Departments of Pediatrics, University of Michigan Medical Center, Ann Arbor en_US
dc.identifier.pmid 7505343 en_US
dc.description.bitstreamurl http://deepblue.lib.umich.edu/bitstream/2027.42/50227/1/490360212_ftp.pdf en_US
dc.identifier.doi http://dx.doi.org/10.1002/jnr.490360212 en_US
dc.identifier.source Journal of Neuroscience Research en_US
dc.owningcollname Interdisciplinary and Peer-Reviewed
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