@article{oai:kanazawa-u.repo.nii.ac.jp:00014129,
 author = {Liang, Guoxin and Liu, Guangyan and Kitamura, Kouichi and Wang, Zhe and Chowdhury, Sajeda and Md Monjurul, Ahasan and Wakae, Kousho and Koura, Miki and Shimadu, Miyuki and Kinoshita, Kazuo and Muramatsu, Masamichi},
 issue = {4},
 journal = {PLoS Pathogens},
 month = {Apr},
 note = {Transforming growth factor (TGF)-β inhibits hepatitis B virus (HBV) replication although the intracellular effectors involved are not determined. Here, we report that reduction of HBV transcripts by TGF-β is dependent on AID expression, which significantly decreases both HBV transcripts and viral DNA, resulting in inhibition of viral replication. Immunoprecipitation reveals that AID physically associates with viral P protein that binds to specific virus RNA sequence called epsilon. AID also binds to an RNA degradation complex (RNA exosome proteins), indicating that AID, RNA exosome, and P protein form an RNP complex. Suppression of HBV transcripts by TGF-β was abrogated by depletion of either AID or RNA exosome components, suggesting that AID and the RNA exosome involve in TGF-β mediated suppression of HBV RNA. Moreover, AID-mediated HBV reduction does not occur when P protein is disrupted or when viral transcription is inhibited. These results suggest that induced expression of AID by TGF-β causes recruitment of the RNA exosome to viral RNP complex and the RNA exosome degrades HBV RNA in a transcription-coupled manner. © 2015 Liang et al.},
 title = {TGF-β Suppression of HBV RNA through AID-Dependent Recruitment of an RNA Exosome Complex},
 volume = {11},
 year = {2015}
}