HTLV-1 Tax-induced NF{kappa}B activation is independent of Lys-63-linked-type polyubiquitination
- Division of Cellular and Molecular Biology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Shirokane-dai, Minato-ku, Tokyo 108-8639 (Japan)
- Division of Immunology, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa 903-0213 (Japan)
- Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Yamada-oka, Suita, Osaka 565-0871 (Japan)
- Human Gene Sciences Center, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113-8510 (Japan)
- Department of Microbiology, Kansai Medical University, Fumizono-cho, Moriguchi, Osaka 570-8506 (Japan)
Human T-cell leukemia virus type 1 (HTLV-1) Tax-induced activation of nuclear factor-{kappa}B (NF{kappa}B) is thought to play a critical role in T-cell transformation and onset of adult T-cell leukemia. However, the molecular mechanism of the Tax-induced NF{kappa}B activation remains unknown. One of the mitogen-activated protein kinase kinase kinses (MAP3Ks) members, TAK1, plays a critical role in cytokine-induced activation of NF{kappa}B, which involves lysine 63-linked (K63) polyubiquitination of NEMO, a noncatalytic subunit of the I{kappa}B kinase complex. Here we show that Tax induces K63 polyubiquitination of NEMO. However, TAK1 is dispensable for Tax-induced NF{kappa}B activation, and deubiquitination of the K63 polyubiquitin chain failed to block Tax-induced NF{kappa}B activation. In addition, silencing of other MAP3Ks, including MEKK1, MEKK3, NIK, and TPL-2, did not affect Tax-induced NF{kappa}B activation. These results strongly suggest that unlike cytokine signaling, Tax-induced NF{kappa}B activation does not involve K63 polyubiquitination-mediated MAP3K activation.
- OSTI ID:
- 20991356
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 357, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2007.03.125; PII: S0006-291X(07)00611-0; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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