2013 Fiscal Year Final Research Report
The role of deubiquitinases USP20 and USP33 in oncogenesis by HTLV-1
Project/Area Number |
23591384
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
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Research Institution | Kyoto University |
Principal Investigator |
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Project Period (FY) |
2011 – 2013
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Keywords | 血液腫瘍学 / ウイルス発がん |
Research Abstract |
Human T-cell leukemia virus type 1 (HTLV-1) is an etiological agent of adult T-cell leukemia (ATL). It has been reported that a cellular deubiquitinase USP20 is a negative regulator of the NF-kappaB signaling pathway, and suppresses proliferation of ATL cells, while its expression is down-regulated in ATL cells. Those observations suggest that USP20 is involved in leukemogenesis of ATL. In this project, we found that USP20 and its relative, USP33, could bind to p53 and activate its transcriptional activity. In addition, it was shown that two viral oncoproteins encoded in HTLV-1, Tax and HTLV-1 bZIP factor (HBZ), were ubiquitinated and their activity were enhanced by this modification. USP20 reduced their ubiquitination level. It was suggested that down-regulation of USP20 in ATL cells might have a role for maintenance of Tax and HBZ ubiquitination.
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Research Products
(39 results)
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[Journal Article] Characterization of simian T-cell leukemia virus type 1 in naturally infected Japanese macaques as a model of HTLV-1 infection2013
Author(s)
Miura M, Yasunaga J, Tanabe J, Sugata K, Zhao T, Ma G, Miyazato P, Ohshima K, Kaneko A, Watanabe A, Saito A, Akari H, Matsuoka M
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Journal Title
Retrovirology
Volume: 10
Pages: 118
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