. . . . "V-src acts as a dominant gene transforming permissive cells in vitro. More strikingly, v-src triggers oncogenesis in vivo, even when inoculated as cloned DNA. To study src gene functions we have used an experimental model comprising different molecularlycloned src oncogenes derived from rather rare events:integration, into the mammalian genome, of a proviral structure corresponding to v-src mRNA (LTR,v-src,LTR); viral transduction of the c-src with the only mutation resulting in a frame shift, thus giving rise to a new oncogene PR2257src. For in vivo experiments we have used a unique system of congenic chicken lines differing only in certain MHC(B) alleles conferring relative resistance or susceptibility to src induced oncogenesis. We have recentlyestablished, from chicken v-src induced tumors, tumor cell lines permanently growing in vitro. Our preliminary results revealed some deletions in the p53 core domain of two long-passaged tumor cell lines. In the proposed project we would like to address"@en . . . . "V-src oncogenes the dominant players in a hierarchy of events leading to cancer"@en . "Vliv ku\u0159ec\u00EDho c-src 3'UTR na genovou expresi jsme zkoumali s pomoc\u00ED aktiva\u010Dn\u00EDch mutant ku\u0159ec\u00EDho genu c-src. 3'UTR sni\u017Euje tumorigenn\u00ED potenci\u00E1l PR2257v-src in vivo u ku\u0159at. To odpov\u00EDd\u00E1 n\u00E1lezu, \u017Ee c-src 3'UTR redukuje mno\u017Estv\u00ED Src proteinu, \u00FArove\u0148 mRNA a"@cs . "2008-06-02+02:00"^^ . . "http://www.isvav.cz/projectDetail.do?rowId=GA204/02/0407"^^ . . . . "The chicken c-src 3'UTR effects on gene expression have been explored using the activated mutants of the chicken c-src gene. 3'UTR decreased the in vivo tumorigenic potential of the PR2257v-src in chickens.This corresponds with the finding that the 3'UTR"@en . . "1"^^ . . . . . "Onkogeny v-src a jejich dominantn\u00ED \u00FAloha v hierarchii ud\u00E1lost\u00ED vedouc\u00EDch k n\u00E1dorov\u00E9mu onemocn\u011Bn\u00ED" . "4"^^ . "0"^^ . . "V-src p\u016Fsob\u00ED jako dominantn\u00ED gen, kter\u00FD transformuje permisivn\u00ED bu\u02C7nky in vitro. P\u0159ekvapuj\u00EDc\u00ED je, \u017Ee v-src spou\u0161t\u00ED onkogenezi in vivo, a to dokonce i v p\u0159\u00EDpad\u011B, \u017Ee je inokulov\u00E1n ve form\u011B klonovan\u00E9 DNA. Ke studiu funkce src genu jsme pou\u017Eili experiment\u00E1ln\u00ED model zahrnuj\u00EDc\u00ED r\u016Fzn\u00E9 molekul\u00E1rn\u011B klonovan\u00E9 onkogeny src, kter\u00E9 byly odvozeny na z\u00E1klad\u011B vz\u00E1cn\u00FDch p\u0159\u00EDpad\u016F integrace provirov\u00E9 struktury odpov\u00EDdaj\u00EDc\u00ED v-src mRNA do sav\u010D\u00EDho genomu (LTR,v-src,LTR), \u010Di virov\u00E9 transdukce c-src s jedinou mutac\u00ED, kter\u00E1 posunula \u010Dtec\u00ED r\u00E1mec a dala vzniknout nov\u00E9mu onkogenu PR2257src. Pro in vivo experimenty pou\u017E\u00EDv\u00E1me syst\u00E9m kongenn\u00EDch lini\u00ED slepic, kter\u00E9 se li\u0161\u00ED v MHC(B) alel\u00E1ch, kter\u00E9 podmi\u0148uj\u00ED rezistenci k onkogenezi vyvolan\u00E9 src. Ned\u00E1vno se n\u00E1m poda\u0159iloetablovat, z ku\u0159ec\u00EDch v-src n\u00E1dor\u016F, bun\u011B\u010Dn\u00E9 n\u00E1dorov\u00E9 linie, kter\u00E9 rostou permanentn\u011B in vitro. P\u0159edb\u011B\u017En\u00E9 v\u00FDsledky uk\u00E1zaly u dvou z t\u011Bchto bun\u011B\u010Dn\u00FDch lini\u00ED delece v centr\u00E1ln\u00ED dom\u00E9n\u011B ku\u0159ec\u00EDho p53. V navrhovan\u00E9m projektu se zam\u011B\u0159\u00EDme na tyto ot\u00E1zky: - jsou" . . . "4"^^ . "Neuvedeno."@en . "0"^^ . . "GA204/02/0407" . .