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10.1073/pnas.1525022113

http://scihub22266oqcxt.onion/10.1073/pnas.1525022113
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suck abstract from ncbi


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pmid27582466
      Proc+Natl+Acad+Sci+U+S+A 2016 ; 113 (37 ): 10388-93
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  • Long noncoding RNA #32 contributes to antiviral responses by controlling interferon-stimulated gene expression #MMPMID27582466
  • Nishitsuji H ; Ujino S ; Yoshio S ; Sugiyama M ; Mizokami M ; Kanto T ; Shimotohno K
  • Proc Natl Acad Sci U S A 2016[Sep]; 113 (37 ): 10388-93 PMID27582466 show ga
  • Despite the breadth of knowledge that exists regarding the function of long noncoding RNAs (lncRNAs) in biological phenomena, the role of lncRNAs in host antiviral responses is poorly understood. Here, we report that lncRNA#32 is associated with type I IFN signaling. The silencing of lncRNA#32 dramatically reduced the level of IFN-stimulated gene (ISG) expression, resulting in sensitivity to encephalomyocarditis virus (EMCV) infection. In contrast, the ectopic expression of lncRNA#32 significantly suppressed EMCV replication, suggesting that lncRNA#32 positively regulates the host antiviral response. We further demonstrated the suppressive function of lncRNA#32 in hepatitis B virus and hepatitis C virus infection. lncRNA#32 bound to activating transcription factor 2 (ATF2) and regulated ISG expression. Our results reveal a role for lncRNA#32 in host antiviral responses.
  • |Activating Transcription Factor 2/*genetics/metabolism [MESH]
  • |Cardiovirus Infections/genetics/virology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Encephalomyocarditis virus/genetics/pathogenicity [MESH]
  • |Gene Expression Regulation [MESH]
  • |Gene Silencing [MESH]
  • |Hepacivirus/genetics/pathogenicity [MESH]
  • |Hepatitis C/genetics/virology [MESH]
  • |Hepatocytes/metabolism/virology [MESH]
  • |Host-Pathogen Interactions/*genetics [MESH]
  • |Humans [MESH]
  • |Interferon Type I/*genetics/metabolism [MESH]
  • |RNA, Long Noncoding/*genetics/metabolism [MESH]
  • |Signal Transduction/genetics [MESH]


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