| First Author | Wood TG | Year | 1984 |
| Journal | Proc Natl Acad Sci U S A | Volume | 81 |
| Issue | 24 | Pages | 7817-21 |
| PubMed ID | 6096859 | Mgi Jnum | J:7699 |
| Mgi Id | MGI:56168 | Doi | 10.1073/pnas.81.24.7817 |
| Citation | Wood TG, et al. (1984) Mouse c-mos oncogene activation is prevented by upstream sequences. Proc Natl Acad Sci U S A 81(24):7817-21 |
| abstractText | Although the molecularly cloned mouse c-mos oncogene locus can be efficiently activated by insertion of a retroviral long terminal repeat (LTR) 5' to its coding region, only low-frequency transformation occurs with the LTR element inserted 3' to this region. Analysis of several of the latter transformed cell lines suggested that loss of 2 kilobases (kb) of normal mouse DNA sequences preceding c-mos was required for oncogene activation. The determination of the transforming potential of deletion mutants containing only portions of this region followed by analysis of their nucleotide sequences identified a region termed upstream mouse sequence (UMS) as a cis-acting locus that prevents c-mos activation by a 3' LTR. The UMS region is approximately 1 kb in length and is located 0.8-1.8 kb upstream from the first ATG in the open reading frame of c-mos. Insertion of UMS 5' to the v-mos coding region also prevents 3' LTR enhancement of its transforming activity, but this inhibition is position dependent and functions only when inserted between v-mos and its putative promoter. The results presented here suggest that UMS may function to regulate c-mos proto-oncogene expression and may explain the lack of detectable c-mos transcripts in normal mouse cells. |
