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Journal of Virology, April 2009, p. 3238-3248, Vol. 83, No. 7
0022-538X/09/$08.00+0 doi:10.1128/JVI.01824-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Molecular Virology Section, Laboratory of Molecular, Microbiology, the National Institute of Allergy and Infectious Diseases, the National Institutes of Health, Bethesda, Maryland 20892-0460,1 Université Montpellier 1 and CNRS, UM5236, Centre d'Études d'Agents Pathogènes et Biotechnologies pour la Santé, Montpellier F-34965, France,2 Université Montpellier 2, Centre d'Études d'Agents Pathogènes et Biotechnologies pour la Santé, Montpellier F-34095, France3
Received 29 August 2008/ Accepted 14 January 2009
Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus etiologically causal of adult T-cell leukemia (ATL). The virus encodes a Tax oncoprotein that functions in transcriptional regulation, cell cycle control, and transformation. ATL is a highly virulent cancer that is resistant to chemotherapeutic treatments. To understand this disease better, it is important to comprehend how HTLV-1 promotes cellular growth and survival. Tax activation of NF-
B is important for the proliferation and transformation of virus-infected cells. We show here that prolyl isomerase Pin1 is over expressed in HTLV-1 cell lines; Pin1 binds Tax and regulates Tax-induced NF-
B activation.
Published ahead of print on 21 January 2009.
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