Association of anti-hepatitis B virus pathway with carcinogenesis
| Project/Area Number |
21790654
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kanazawa University |
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Principal Investigator |
KITAMURA Kouichi Kanazawa University, 医学系, 助教 (70378892)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ウイルス / がん / ゲノム / 免疫学 / ウィルス / 癌 |
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| Research Abstract |
Human APOBEC3 proteins are reported to be antiviral factors and catalyze C-to-U conversion on hepatitis B virus (HBV) DNA by cytosine deamination. Extensive G-to-A hypermutation on plus-strand of HBV DNA has been observed from APOBEC3G-expressing hepatoma cells. We investigated whether UNG also process the hypermutated HBV genome with base excision activity. We found that the UNG inhibition caused accumulation of hypermutation in nuclear cccDNA and decrease of cytoplasmic rcDNA level. Sequencing analysis showed that some of these cccDNA mutations resulted in nonsense codons within viral polymerase coding region. These results suggest that the BER pathway triggered from nuclear UNG repairs the viral DNA mutations introduced by the antiviral APOBECs.
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Report
(3 results)
Research Products
(10 results)
