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. © 2003 Elsevier Inc. All rights reserved.
Boyapati, A., Wilson, M., Yu, J., & Rundell, K. (2003). SV40 17KT antigen complements dnaj mutations in large T antigen to restore transformation of primary human fibroblasts. Virology, 315(1), 148–158. https://doi.org/10.1016/S0042-6822(03)00524-5