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Originally published In Press as doi:10.1074/jbc.M110885200 on February 27, 2002

J. Biol. Chem., Vol. 277, Issue 19, 17231-17238, May 10, 2002
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Insulin Receptor Substrate 1 Translocation to the Nucleus by the Human JC Virus T-antigen*

Adam LassakDagger , Luis Del ValleDagger , Francesca Peruzzi, Jin Ying Wang, Sahnila Enam, Sidney Croul, Kamel Khalili, and Krzysztof Reiss§

From the Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania 19122

Insulin receptor substrate 1 (IRS-1) is the major signaling molecule for the insulin and insulin-like growth factor 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 JC virus 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 JC virus T-antigen-transformed cells in anchorage-independent culture conditions. 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.

* This work was supported by National Institutes of Health Grant PO1 NS 36466.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger These authors contributed equally to this work.

§ To whom correspondence should be addressed: Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, 1900 North 12th St., Biology Life Science Bldg., Rm. 238, Philadelphia, PA 19122. Tel.: 215-204-0620; Fax: 215-204-0679; E-mail: kreiss@astro.temple.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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