Volume 8 Supplement 1

15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

HTLV-1 Tax-induced NF-κB activation is negatively regulated by Ubiquitin-specific peptidase 20 (USP20)

  • Junichiro Yasunaga1Email author,
  • Frank C Lin1,
  • Xiongbin Lu2 and
  • Kuan-Teh Jeang1
Retrovirology20118(Suppl 1):A129

https://doi.org/10.1186/1742-4690-8-S1-A129

Published: 6 June 2011

Human T cell leukemia virus type 1 (HTLV-1) causes a fatal hematopoietic malignancy, adult T cell leukemia (ATL), and a viral oncoprotein Tax is considered to play the important roles in leukemogenesis through its potent activation of NF-κB. Protein ubiquitination is crucial for the proper regulation of NF-κB pathway. It is also known that the function of Tax is modified by ubiquitination, indicating that ubiquitination machineries contribute to the oncogenic mechanisms of ATL. We report that two ubiquitin-specific peptidases, USP20 and USP33, deubiquitinate TRAF6 and suppress IL-1β-induced NF-κB activation. We find that USP20 deubiquitinates Tax and inhibits Tax-induced NF-κB activation, consistent with Tax being a substrate of USP20. In HTLV-1-transformed cells, the transcription of USP20 is reduced compared with HTLV-1-negative T cells, and ectopic USP20 expression was found to inhibit the proliferation of an HTLV-1-transformed cell line, MT4. Our findings suggest USP20 is a key negative regulator of NF-κB signaling and can influence HTLV-1-induced leukemogenesis.

Authors’ Affiliations

(1)
Molecular Virology Section, Laboratory of Molecular Microbiology, NIAID, NIH
(2)
University of Texas MD Anderson Cancer Center

Copyright

© Yasunaga et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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