Ubiquitin-specific peptidase 20 targets TRAF6 and human T cell leukemia virus type 1 tax to negatively regulate NF-kappaB signaling.
NF-κB plays a key role in innate and acquired immunity. Its activity is regulated through intricate signaling networks. Persistent or excessive activation of NF-κB induces diseases, such as autoimmune disorders and malignant neoplasms. Infection by human T cell leukemia virus type 1 (HTLV-1) causes a fatal hematopoietic malignancy termed adult ... T cell leukemia (ATL). The HTLV-1 viral oncoprotein Tax functions pivotally in leukemogenesis through its potent activation of NF-κB. Recent findings suggest that protein ubiquitination is crucial for proper regulation of NF-κB signaling and for Tax activity. Here, we report that ubiquitin-specific peptidase USP20 deubiquitinates TRAF6 and Tax and suppresses interleukin 1β (IL-1β)- and Tax-induced NF-κB activation. Our results point to USP20 as a key negative regulator of Tax-induced NF-κB signaling.
Mesh Terms:
Cell Line, Gene Expression Regulation, Gene Expression Regulation, Viral, Gene Products, tax, HeLa Cells, Human T-lymphotropic virus 1, Humans, Interleukin-1, Jurkat Cells, NF-kappa B, Signal Transduction, T-Lymphocytes, TNF Receptor-Associated Factor 6, Ubiquitin Thiolesterase
Cell Line, Gene Expression Regulation, Gene Expression Regulation, Viral, Gene Products, tax, HeLa Cells, Human T-lymphotropic virus 1, Humans, Interleukin-1, Jurkat Cells, NF-kappa B, Signal Transduction, T-Lymphocytes, TNF Receptor-Associated Factor 6, Ubiquitin Thiolesterase
J. Virol.
Date: Jul. 01, 2011
PubMed ID: 21525354
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