Transactivation of BKV and SV40 early promoters by BKV and SV40 T-antigens.
The early promoters of BKV and SV40 plasmids were transactivated in both BKV and SV40-transformed cells which failed to support replication of these plasmids. This suggests that the T-antigen of either virus can transactivate BKV and SV40 early promoters by either increasing the availability of cellular transcription factors or by directly interacting with specific sequences which comprise the transcriptional control region of the early promoters. We also observed that removal of 8-bp on the early side of T-antigen binding site I of BKV does not alter viral-plasmid replication.
D000818:Animals; D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor / Q000378:metabolism*; D001739:BK Virus / Q000235:genetics*; D002460:Cell Line; D002472:Cell Transformation, Viral; D002795:Choline O-Acetyltransferase / Q000235:genetics; D000882:Haplorhini; D009856:Oncogene Proteins, Viral / Q000378:metabolism*; D027383:Papillomaviridae / Q000235:genetics*; D010957:Plasmids; D027382:Polyomaviridae; D011120:Polyomavirus / Q000235:genetics*; D011401:Promoter Regions, Genetic; D011995:Recombination, Genetic; D013539:Simian virus 40 / Q000235:genetics*; D014779:Virus Replication
D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor; D009856:Oncogene Proteins, Viral; D002795:Choline O-Acetyltransferase