作者: H. Iba , T. Takeya , F. R. Cross , T. Hanafusa , H. Hanafusa
关键词:
摘要: Abstract The transforming activity of the cellular src (c-src) gene as well hybrid genes between viral and was tested by constructing derivatives Rous sarcoma virus DNA in which all or part (v-src) replaced corresponding portion c-src gene. After these were introduced into chicken embryo fibroblasts transfection, replication-competent recovered, induced expression p60src at a level equivalent to p60v-src cells infected with wild type. Replacement v-src gene, either upstream downstream Bgl I site, homologous resulted fully viruses. On other hand, stock obtained from transfected containing entire had very low titer focus-forming virus, while it contained high infectious virus. We present evidence that rare small foci are formed mutant viruses generated original c-src-containing These results indicate overproduction product does not cause cell transformation, this proto-oncogene is subject relatively rate mutation when incorporated retrovirus genome, resulting acquisition capacity.