| First Author | Hraba-Renevey S | Year | 1989 |
| Journal | Oncogene | Volume | 4 |
| Issue | 5 | Pages | 601-8 |
| PubMed ID | 2542864 | Mgi Jnum | J:20468 |
| Mgi Id | MGI:68560 | Citation | Hraba-Renevey S, et al. (1989) SV40-induced expression of mouse gene 24p3 involves a post-transcriptional mechanism. Oncogene 4(5):601-8 |
| abstractText | SV40 and polyoma virus induce a mitotic host reaction in confluent, Go-arrested primary mouse kidney cell cultures. To define the primary effects of infection we constructed a cDNA library corresponding to polyA+ mRNA isolated shortly after onset of polyoma T-antigen synthesis. By differential screening of the library we have isolated and then sequenced cDNA recombinant 24p3; determined by Northern blotting, 24p3 mRNA steady state levels increased in parallel with polyoma and SV40 T-antigen synthesis. Since this rapid and early increase was particularly striking (14-20 fold) in SV40-infected cells, we studied the molecular mechanism of induction in this virus-cell system. We show that wt SV40 large T-antigen is required for the increase in 24p3 mRNA levels. The results tend to exclude that this increase is due to an SV40-induced stabilization of the 24p3 mRNA, or to an SV40-induced stimulation of transcription of the 24p3 gene; they are compatible with the working hypothesis that SV40 large T-antigen increases the efficiency of processing, possibly splicing, of the 24p3 pre-mRNA. The biological implications of these results are discussed. |
