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

  • Boyapati A
  • Wilson M
  • Yu J
 et al. 
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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.

Author-supplied keywords

  • 17KT antigen
  • Human fibroblasts
  • SV40
  • Transformation
  • dnaJ

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Authors

  • Anita Boyapati

  • Marlena Wilson

  • Jing Yu

  • Kathleen Rundell

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