trans-activation of cellular and viral promoters by a transforming nonkaryophilic simian virus 40 large T antigen.
We used the chloramphenicol acetyl transferase (CAT) transient expression system to study the transactivating ability of a simian virus 40 (SV40) mutant that was unable to transport and localize large T antigen into the nucleus and which retained the competence to transform established cell lines. The effect of the SV40 wild type and the SV40 mutant for the large T antigen was tested in both mouse and simian cells on a series of plasmids in which the CAT gene was regulated by one of the following promoters: SV40 early and late, herpes simplex virus thymidine kinase, chicken alpha 2(I) collagen, mouse H-2Kk. Our results indicated that both the SV40 wild type and the cytoplasmic mutant for the large T antigen regulated transcription from any promoter tested, suggesting that the trans-activation by SV40 does not require the nuclear localization of the 100,000-molecular-weight large T-antigen protein.
D000818:Animals; D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor / Q000235:genetics / Q000378:metabolism*; D002460:Cell Line; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D005814:Genes, Viral; D009154:Mutation; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D011494:Protein Kinases / Q000378:metabolism*; D013539:Simian virus 40 / Q000235:genetics*; D014775:Virus Activation
D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor; D009856:Oncogene Proteins, Viral; D011494:Protein Kinases