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pubmed-article:9742130pubmed:abstractTextBy using a model system for cell transformation mediated by the cooperation of the activated H-ras oncogene and the inactivated p53 tumor suppressor gene, rCop-1 was identified by mRNA differential display as a gene whose expression became lost after cell transformation. Homology analysis indicates that rCop-1 belongs to an emerging cysteine-rich growth regulator family called CCN, which includes connective-tissue growth factor, CYR61, CEF10 (v-src inducible), and the product of the nov proto-oncogene. Unlike the other members of the CCN gene family, rCop-1 is not an immediate-early gene, it lacks the conserved C-terminal domain which was shown to confer both growth-stimulating and heparin-binding activities, and its expression is lost in cells transformed by a variety of mechanisms. Ectopic expression of rCop-1 by retroviral gene transfers led to cell death in a transformation-specific manner. These results suggest that rCop-1 represents a new class of CCN family proteins that have functions opposing those of the previously identified members.lld:pubmed
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pubmed-article:9742130pubmed:articleTitleIdentification of rCop-1, a new member of the CCN protein family, as a negative regulator for cell transformation.lld:pubmed
pubmed-article:9742130pubmed:affiliationVanderbilt Cancer Center, Department of Cell Biology, Vanderbilt University, Nashville, Tennessee 37232, USA.lld:pubmed
pubmed-article:9742130pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9742130pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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