Tham khảo tài liệu 'báo cáo hóa học: " rotavirus nonstructural protein 1 antagonizes innate immune response by interacting with retinoic acid inducible gene i"', luận văn - báo cáo phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả | Virology Journal BioMed Central Vz The Open Access Publisher This Provisional PDF corresponds to the article as it appeared upon acceptance. Fully formatted PDF and full text HTML versions will be made available soon. Rotavirus nonstructural protein 1 antagonizes innate immune response by interacting with retinoic acid inducible gene I Virology Journal 2011 8 526 doi 1743-422X-8-526 Lan Qin qinlan99@ Lili Ren renlili@ Zhuo Zhou zhouzhuo@ Xiaobo Lei fyleixb@ Lan Chen lan01128@ Qinghua Xue xueqh114@ Xinlei Liu liu228783@ Jianwei Wang wangjw28@ Tao Hung hongt@ ISSN 1743-422X Article type Research Submission date 23 August 2011 Acceptance date 8 December 2011 Publication date 8 December 2011 Article URL http content 8 1 526 This peer-reviewed article was published immediately upon acceptance. It can be downloaded printed and distributed freely for any purposes see copyright notice below . Articles in Virology Journal are listed in PubMed and archived at PubMed Central. For information about publishing your research in Virology Journal or any BioMed Central journal go to http authors instructions For information about other BioMed Central publications go to http 2011 Qin et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Rotavirus nonstructural protein 1 antagonizes innate immune response by interacting with retinoic acid inducible gene I ArticleCategory Research ArticleHistory Received 23-Aug-2011 Accepted 16-Nov-2011 ArticleCopyright 2011 Qin et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution .
