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 Blood, 1 February 2007, Vol. 109, No. 3, pp. 1051-1060.
Prepublished online as a Blood First Edition Paper on September 21, 2006; DOI 10.1182/blood-2006-06-026781.

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Submitted June 1, 2006
Accepted September 18, 2006

Human T-cell leukemia virus type-1 Tax oncoprotein regulates G protein signaling

Jean-Claude Twizere*, Jean-Yves Springael, Mathieu Boxus, Arsene Burny, Franck Dequiedt, Jean-Francois Dewulf, Julie Duchateau, Daniel Portetelle, Patrice Urbain, Carine Van Lint, Patrick L Green, Renaud Mahieux, Marc Parmentier, Luc Willems, and Richard Kettmann

Cellular and Molecular Biology, Faculty of Gembloux, Gembloux, Belgium
Recherche en Biologie Humaine et Moleculaire, Universite Libre de Bruxelles, Brussels, Belgium
Laboratoire de Virologie Moleculaire, IBMM, Universite Libre de Bruxelles, Brussels, Belgium
Comprehensive Cancer Center and Solove Research Institute, The Ohio State University, Columbus, OH
Unite d'Epidemiologie et Physiopathologie des Virus Oncogenes, Institut Pasteur, Paris, France

* Corresponding author; email: twizere.jc{at}fsagx.ac.be.

Human T-cell leukemia virus type-1 (HTLV-1) is associated with adult T-cell leukemia (ATL) and neurological syndromes. HTLV-1 encodes the oncoprotein Tax-1 that modulates viral and cellular gene expression leading to T-cell transformation. Guanine nucleotide binding proteins (G proteins) and G protein-coupled receptors (GPCRs) constitute the largest family of membrane proteins known and are involved in the regulation of most biological functions. Here, we report an interaction between HTLV-I Tax oncoprotein and the G protein {beta} subunit. Interestingly, while the G protein {beta} subunit inhibits Tax-mediated viral transcription, Tax-1 perturbs G protein {beta} subcellular localization. Functional evidence for these observations was obtained using conditional Tax-1-expressing transformed T-lymphocytes, where Tax expression correlated with activation of the SDF-1/CXCR4 axis. Our data indicated that HTLV-1 has developed a strategy based on the activation of the SDF-1/CXCR4 axis in the infected cell, which could have tremendous implications for new therapeutic strategies.


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