Disruption of signaling responsed to stress by HTLV-1 bZIP factor
| Project/Area Number |
26430128
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ウイルス / HTLV-1 / HBZ / 発がん / 翻訳後修飾 / 転写制御 / 細胞死 / ユビキチン / ヒストン修飾 / 生体防御 / オートファジー / ウイルス性発がん / 白血病 / mTOR / ATL |
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| Outline of Final Research Achievements |
Human T-cell leukemia virus type-1 (HTLV-1) infection causes adult T-cell leukemia (ATL). The viral protein HTLV-1 HBZ is thought to be associated with the development of ATL. We focused to cellular function of HBZ and defined the following two 2 points. 1), HBZ and CENP-B associate with their central regions in cells. Furthermore, overexpression of HBZ abrogated the DNA-binding activity of CENP-B to the α-satellite DNA region containing the CENP-B box motif, which in turn inhibited the CENP-B-mediated trimethylation of histone H3K9 in T-cells. 2), HBZ interacted with cullin 1 (CUL1) through a head-to-tail and the expression of HBZ in cells stabilized MCL1 protein expression.
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Report
(4 results)
Research Products
(11 results)
