Research on the mechanism of tumorigenesis by A20 dysfunction in HCV-infected B cells
| Project/Area Number |
23659177
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
KUSUNOKI Hideki 国立感染症研究所, 血液・安全性研究部, 主任研究官 (90334060)
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| Co-Investigator(Renkei-kenkyūsha) |
MIZUOCHI Toshiaki 国立感染症研究所, 血液・安全性研究部, 室長 (30135701)
OKUMA Kazu 国立感染症研究所, 血液・安全性研究部, 室長 (80315085)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | A20 / B 細胞リンパ腫 / HCV 感染 / 分子腫瘍学 / B細胞リンパ腫 / HCV感染 |
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| Research Abstract |
In this study, we investigated the mechanism of tumorgenesis by A20 dysfunction in HCV-infected B cells. We found that A20, a negative regulator of the canonical NF-κB pathway, was dramatically enhanced and partially cleaved in HCV-infected B cells. When the possibility of A20 cleavage by HCV NS3 protease was examined, the direct result, which shows the A20 cleavage by its protease, was not obtained. We also found that MALT1 was enhanced in CHC B cells. Thus, this observation suggests that enhanced expression of MALT1 in HCV-infected B cells may cleave A20.
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Report
(3 results)
Research Products
(4 results)
