SV40 17KT antigen complements dnaj mutations in large T antigen to restore transformation of primary human fibroblasts

24Citations
Citations of this article
5Readers
Mendeley users who have this article in their library.
Get full text

Abstract

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.

Cite

CITATION STYLE

APA

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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free