Activation of the transforming potential of a normal cell sequence: a molecular model for oncogenesis.
The molecularly cloned, long terminal repeat (LTR) of the Moloney sarcoma virus (M-MSV) provirus has been covalently linked to c-mos, the cellular homolog of the M-MSV-specific sequence, v-mos. These newly constructed clones lack any M-MSV-derived sequences other than the LTR, but in DNA transfection assays they transform cells as efficiently as cloned subgenomic M-MSV fragments containing both v-mos and LTR. Cells transformed by LTR:c-mos hybrid molecules contain additional copies of mos DNA, and several size classes of polyadenylated RNA's with sequence homology to mos. The activation of the transforming potential of c-mos by the proviral LTR suggests a model whereby LTR-like elements could activate other normal cell sequences with oncogenic potential.
D000818:Animals; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D004274:DNA, Recombinant; D003673:Defective Viruses / Q000235:genetics; D005786:Gene Expression Regulation; D005814:Genes, Viral; D051379:Mice; D008979:Moloney murine leukemia virus / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D009876:Operon; D010957:Plasmids
D004274:DNA, Recombinant