Journal
VIROLOGY
Volume 403, Issue 2, Pages 173-180Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2010.04.018
Keywords
HTLV-1; Bcl3; PI3K; AKT; Post-transcriptional mechanisms
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Funding
- Japan Society for the Promotion of Science (JSPS) [20790359]
- Ministry of Health, Labor and Welfare of Japan
- Kanazawa Medical University [S2007-7, S2008-11]
- Grants-in-Aid for Scientific Research [20790359, 22790439] Funding Source: KAKEN
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Bcl3 is a member of the I kappa B family that regulates genes involved in cell proliferation and apoptosis. Recent reports indicated that Bcl3 is overexpressed in HTLV-1-infected T cells via Tax-mediated transactivation, and acts as a negative regulator of viral transcription. However, the role of Bcl3 in cellular signal transduction and the growth of HTLV-1-infected T cells have not been reported. In this study, we showed that the knockdown of Bcl3 by short hairpin RNA inhibited the growth of HTLV-1-infected T cells. Although phosphatidylinositol-3 kinase (PI3K) inhibitor reduced Bcl3 expression, inactivation of glycogen synthase kinase 3 (GSK3), an effector kinase of the PI3K/Akt signaling pathway, restored Bcl3 expression in Tax-negative but not in Tax-positive T cells. Our results indicate that the overexpression of Bcl3 in HTLV-1-infected T cells is regulated not only by transcriptional but also by post-transcriptional mechanisms, and is involved in overgrowth of HTLV-1-infected T cells. (C) 2010 Elsevier Inc. All rights reserved.
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