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pubmed:abstractText |
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.
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