期刊
FEBS LETTERS
卷 587, 期 18, 页码 3148-3152出版社
WILEY
DOI: 10.1016/j.febslet.2013.07.055
关键词
AID; APOBEC; Base excision repair; Hepatitis B virus; cccDNA
资金
- Funding Program for Next Generation World-Leading Researchers (NEXT project)
- MEXT KAKENHI [20012018]
- JSPS KAKENHI of Japan [21790654, 23790780]
- Grants-in-Aid for Scientific Research [20012018, 21790654, 23790780] Funding Source: KAKEN
Covalently closed circular DNA (cccDNA) forms a template for the replication of hepatitis B virus (HBV) and duck HBV (DHBV). Recent studies suggest that activation-induced cytidine deaminase (AID) functions in innate immunity, although its molecular mechanism of action remains unclear, particularly regarding HBV restriction. Here we demonstrated that overexpression of chicken AID caused hypermutation and reduction of DHBV cccDNA levels. Inhibition of uracil-DNA glycosylase (UNG) by UNG inhibitor protein (UGI) abolished AID-induced cccDNA reduction, suggesting that the AID/UNG pathway triggers the degradation of cccDNA via cytosine deamination and uracil excision. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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