| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| 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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