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dc.contributor.authorRam, Tracy G.en_US
dc.contributor.authorKokeny, Kristine E.en_US
dc.contributor.authorDilts, Cheryl A.en_US
dc.contributor.authorEthier, Stephen P.en_US
dc.date.accessioned2007-04-06T18:05:13Z
dc.date.available2007-04-06T18:05:13Z
dc.date.issued1995-06en_US
dc.identifier.citationRam, Tracy G.; Kokeny, Kristine E.; Dilts, Cheryl A.; Ethier, Stephen P. (1995)."Mitogenic activity of neu differentiation factor/heregulin mimics that of epidermal growth factor and insulin-like growth factor-I in human mammary epithelial cells." Journal of Cellular Physiology 163(3): 589-596. <http://hdl.handle.net/2027.42/49890>en_US
dc.identifier.issn0021-9541en_US
dc.identifier.issn1097-4652en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/49890
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7775601&dopt=citationen_US
dc.description.abstractRecently, a family of growth factors has been described that activates erbB-2 receptors. These factors, known as the neu differentiation factors (NDF) or heregulins (HRG), induce tyrosine phosphorylation of erbB-2 receptors as a result of their direct interaction with either erbB-3 or erbB-4 receptors. Although it is known that expression of erbB-2 receptors has relevance in human breast cancer progression, how erbB-2, -3 and -4 receptors regulate mammary epithelial cell proliferation is not known. Therefore, experiments were carried out to study the mitogenic activity of NDF/HRG on the human mammary epithelial cell line MCF-10A which can be cultured continuously under serum-free conditions. MCF-10A cells, like primary cultures of normal human mammary epithelial cells, express an absolute requirement for exogenous epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) for growth. The results of these experiments indicate that NDF/HRG can induce tyrosine phosphorylation of p185erbB-2 in MCF-10A cells and is mitogenic for these cells. This is consistent with the coexpression of erbB-2 and erbB-3 mRNA that we have observed in MCF-10A cells. In addition, we found that NDF/HRG can substitute for either EGF or IGF-I to stimulate proliferation of these cells. The ability to substitute for both EGF and IGF-I is a unique property of NDF/HRG and is not shared by other members of the EGF or IGF family of growth factors, nor by other factors that we have studied. A striking isoform specificity was also observed which indicated that the Β-isoforms of NDF/HRG were greater than ten times more mitogenic than the Α-isoforms. We also examined the mitogenic activity of NDF/HRG on MCF-10A cells that overexpress the erbB-2 receptor as a result of infection with a retroviral vector containing the human c-erbB-2 gene (MCF-10AerbB-2 cells). These studies indicated that MCF-10AerbB-2 cells have increased sensitivity to the mitogenic effects of NDF/HRG and that these cells are responsive to the Α-isoforms of NDF/HRG at physiological concentrations. Thus, NDF/HRG is a dual specificity growth factor for human mammary epithelial cells, and the responsiveness of the cells to NDF/HRG is influenced by the level of expression of erbB-2 receptors. © 1995 Wiley-Liss, Inc.en_US
dc.format.extent923770 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherCell & Developmental Biologyen_US
dc.titleMitogenic activity of neu differentiation factor/heregulin mimics that of epidermal growth factor and insulin-like growth factor-I in human mammary epithelial cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelKinesiology and Sportsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Radiation Oncology, Division of Radiation and Cancer Biology, The University of Michigan Medical School, Ann Arbor, Michigan 48109-0582en_US
dc.contributor.affiliationumDepartment of Radiation Oncology, Division of Radiation and Cancer Biology, The University of Michigan Medical School, Ann Arbor, Michigan 48109-0582en_US
dc.contributor.affiliationumDepartment of Radiation Oncology, Division of Radiation and Cancer Biology, The University of Michigan Medical School, Ann Arbor, Michigan 48109-0582en_US
dc.contributor.affiliationumDepartment of Radiation Oncology, Division of Radiation and Cancer Biology, The University of Michigan Medical School, Ann Arbor, Michigan 48109-0582 ; Department of Radiation Oncology, University of Michigan Medical School, 1331 East Ann Street, Ann Arbor, MI 48109-0582en_US
dc.identifier.pmid7775601en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/49890/1/1041630320_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/jcp.1041630320en_US
dc.identifier.sourceJournal of Cellular Physiologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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