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M110885200v1
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Papers In Press, published online ahead of print February 27, 2002
J. Biol. Chem, 10.1074/jbc.M110885200
Submitted on November 13, 2001
Revised on February 12, 2002
Accepted on February 27, 2002

Insulin receptor substrate 1 translocation to the nucleus by the human JC virus T-antigen

Adam Lassak, Luis Del Valle, Francesca Peruzzi, Jin Ying Wang, Sahnila Enam, Sidney Croul, Kamel Khalili, and Krzysztof Reiss

Center for Neurovirology and Cancer Biology, Temple University, Philadelphia, PA 19122

Corresponding Author: kreiss{at}astro.temple.edu

Insulin receptor substrate 1 (IRS-1) is the major signaling molecule for the insulin and insulin-like growth factor I (IGF-I) receptors, which transduces both metabolic and growth-promoting signals, and has transforming properties when overexpressed in the cells. Here we show that IRS-1 is translocated to the nucleus in the presence of the early viral protein - T-antigen of the human polyomavirus JC. Nuclear IRS-1 was detected in T-antigen positive cell lines and in T-antigen positive biopsies from patients diagnosed with medulloblastoma. The IRS-1 domain responsible for a direct JCV T-antigen binding was localized within the N-terminal portion of IRS-1 molecule, and the binding was independent from IRS-1 tyrosine phosphorylation and was strongly inhibited by IRS-1 serine phosphorylation. In addition, competition for the IRS-1 - T-antigen binding by a dominant negative mutant of IRS-1 inhibited growth and survival of JCV T-antigen -transformed cells in anchorage-independent culture condition. Based on these findings, we propose a novel role for the IRS-1 - T-antigen complex in controlling cellular equilibrium during viral infection. It may involve uncoupling of IRS-1 from its surface receptor and translocation of its function to the nucleus.


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