SV40 17KT antigen complements dnaj mutations in large T antigen to restore transformation of primary human fibroblasts.
Transformation of human cells requires both SV40 large T and small t antigens. Plasmids that contained mutations in the amino-terminal dnaJ domain of the early region fail to transform human diploid fibroblasts. However, large T dnaJ mutants can be rescued by plasmids that express early region products other than large T antigen. The protein found to be responsible for such complementation was the third early region product, 17KT. Similar to large T, this protein reduces levels of the retinoblastoma-related protein, p130, and stimulates cell-cycle progression of quiescent fibroblasts, two activities of large T that are disrupted by dnaJ mutations.
Department of Microbiology-Immunology and The Robert H. Lurie Comprehensive Cancer Center, Northwestern University, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Anita
A
Boyapati
Marlena
M
Wilson
Jing
J
Yu
Kathleen
K
Rundell
D000952:Antigens, Polyomavirus Transforming / Q000235:genetics*; D000956:Antigens, Viral / Q000235:genetics* / Q000276:immunology; D002461:Cell Line, Transformed; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D005347:Fibroblasts / Q000821:virology*; D005816:Genetic Complementation Test; D050956:HSP40 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000235:genetics*; D006801:Humans; D009154:Mutation; D013539:Simian virus 40 / Q000235:genetics* / Q000276:immunology
D000952:Antigens, Polyomavirus Transforming; D000956:Antigens, Viral; D050956:HSP40 Heat-Shock Proteins; D006360:Heat-Shock Proteins