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pubmed:abstractText |
Glucocorticoid hormones enhance the transcription of mouse mammary tumor virus DNA by mechanisms involving a direct interaction of the hormone receptor with four binding sites in a glucocorticoid regulatory element located between -72 and -192 base pairs upstream of the main transcription initiation site within the proviral long terminal repeat regions. Methylation at the N-7 position of any of three G residues within one of the binding sites prevents binding of the receptor. In addition, in the presence of the receptor, methylation by dimethyl sulfate is reduced at several G residues, indicating sites of contact between the receptor and DNA at these positions. The G residues in the hexanucleotide 5'-T-G-T-T-C-T-3' 3'-A-C-A-A-G-A-5' were protected by the receptor against MH2-specific gene. (iii) myc is followed by the 3'-terminal c region of about 400 nucleotides, which is colinear with that of Rous sarcoma virus except for a substitution near the 5' end of the long terminal repeat. It is concluded that MH2 contains two genes with oncogenic potential, the delta gag- mht gene, which is closely related to the delta gag-raf transforming gene of MSV 3611, and the myc gene, which is related to the transforming gene of MC29. Furthermore, it may be concluded that the cellular proto-onc genes, which on sequence transduction become viral onc genes, are a small group because among the 19 known onc sequences, 5 are shared by different taxonomic groups of viruses of which the mht /raf homology is the closest determined so far.
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