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Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a
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research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a
Creator
Duan, Yueqiang
Gu, Hongjing
Lai, Chengcai
Wang, Keyu
Wang, Xiliang
Yang, Penghui
Zhao, Zhongpeng
Chen, Runsheng
Wang, Cheng
Zhang,
Cheng, Sijie
Lili,
Lingna,
Liu, Lihui
Liu, Qinghua
Liu, Ziyang
Luo, Jianjun
Song, Jianxun
Xia, Min
Source
BioRxiv; MedRxiv
abstract
Accumulating evidence has shown that long noncoding RNAs (lncRNAs) are involved in several biological processes, including immune responses. However, the role of lncRNAs in antiviral innate immune responses remains largely unexplored. Here, we identify an uncharacterized human lncRNA from influenza A virus (IAV) patients, antivirus and activate neutrophil (AVAN), that is significantly up-regulated upon virus infection. Mechanistically, nuclear lncRNA-AVAN positively regulates the transcription of forkhead box O3A (FOXO3a) by associating with its promoter and inducing chromatin remodeling to promote neutrophil chemotaxis. Furthermore, we also found that cytoplasmic lncRNA-AVAN directly binds tripartite motif containing 25 (TRIM25) and enhances the association of TRIM25 and Retinoic acid inducible gene-1 proteins (RIG-I) and the ubiquitylation of RIG-I, thereby promoting TRIM25- and RIG-I-mediated antiviral innate immune signaling. More importantly, we enforced the expression of AVAN in transgenic mice and found that it significantly alleviated IAV virulence and virus production. Collectively, these findings highlight the potential clinical implications of lncRNA-AVAN as a key positive regulator of the antiviral innate immune response and a promising target for developing broad antiviral therapeutics.
has issue date
2019-04-30
(
xsd:dateTime
)
bibo:doi
10.1101/623132
has license
medrxiv
sha1sum (hex)
42311b11c5256d17559b1bbda5acc951593e6406
schema:url
https://doi.org/10.1101/623132
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Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a
schema:publication
bioRxiv
resource representing a document's body
covid:42311b11c5256d17559b1bbda5acc951593e6406#body_text
is
schema:about
of
named entity 'promising'
named entity 'innate immune responses'
named entity 'lncRNAs'
named entity 'potential'
named entity 'potential'
named entity 'antiviral'
named entity 'RIG-I'
named entity 'immunity'
named entity 'innate immune'
named entity 'positive'
named entity 'forkhead box'
named entity 'noncoding'
named entity 'However'
named entity 'proliferation'
named entity 'AVAN'
named entity 'neutrophil'
named entity 'cis'
named entity 'A549'
named entity 'TRIM25'
named entity 'lncRNAs'
named entity 'cytokine'
named entity 'chemotaxis'
named entity 'virus infection'
named entity 'lncRNAs'
named entity 'lncRNA'
named entity 'antiviral'
named entity 'biological processes'
named entity 'RIG-I'
named entity 'Long noncoding RNA'
named entity 'TRIM25'
named entity 'proliferation'
named entity 'RNAs'
named entity 'endogenous'
named entity 'CXCL2'
named entity 'Kodak'
named entity 'OASL'
named entity 'overexpressing'
named entity 'IAV'
named entity 'IAV'
named entity 'AAV2'
named entity 'lncRNA'
named entity 'type I IFN'
named entity 'IAV'
named entity 'qRT-PCR'
named entity 'inflammatory diseases'
named entity 'reverse transcription'
named entity 'neutrophil'
named entity 'A549'
named entity 'IAV'
named entity 'TRIM25'
named entity 'IAV'
named entity 'overexpressing'
named entity 'Primer pairs'
named entity 'RIG-I'
named entity 'infection'
named entity 'down-regulated'
named entity 'lncRNAs'
named entity 'neutrophil'
named entity 'cytoplasm'
named entity 'p<0.05'
named entity 'Gene ontology'
named entity 'human genome'
named entity 'infection'
named entity 'exogenous'
named entity 'antiviral'
named entity 'nucleus'
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