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10.1111/cmi.13150 http://scihub22266oqcxt.onion/10.1111/cmi.13150 C7162240!7162240 !31876380     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31876380 &cmd=llinks): Failed to open stream: HTTP request failed! 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Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 |pdf=|usr=}}{{31876380 }} gab.com Text Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 JO: Cell Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=31876380 #FOAvip Influenza A virus (IAV) has evolved multiple mechanisms to compromise type I interferon (IFN) responses. The antiviral function of IFN is mainly exerted by activating the JAK/STAT signalling and subsequently inducing IFN-stimulated gene (ISG) production. However, the mechanism by which IAV combat the type I IFN signalling pathway is not fully elucidated. In this study, we explored the roles of human microRNAs modulated by IAV infection in type I IFN responses. We demonstrated that microRNA-30 (miR-30) family members were downregulated by IAV infection. Our data showed that the forced expression of miR-30 family members inhibited IAV proliferation, while miR-30 family member inhibitors promoted IAV proliferation. Mechanistically, we found that miR-30 family members targeted and reduced SOCS1 and SOCS3 expression, and thus relieved their inhibiting effects on IFN/JAK/STAT signalling pathway. In addition, miR-30 family members inhibited the expression of NEDD4, a negative regulator of IFITM3, which is important for host defence against influenza viruses. Our findings suggest that IAV utilises a novel strategy to restrain host type I IFN-mediated antiviral immune responses by decreasing the expression of miR-30 family members, and add a new way to understand the mechanism of immune escape caused by influenza viruses. Twit Text FOAVip Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 ????Cell Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=31876380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31876380 #FOAvip English Wikipedia <ref>{{Cite pmid|31876380 }}</ref> Human microRNA-30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 #MMPMID31876380 Lin X ; Yu S ; Ren P ; Sun X ; Jin M Cell Microbiol 2020[May]; 22 (5 ): e13150 PMID31876380 show ga Influenza A virus (IAV) has evolved multiple mechanisms to compromise type I interferon (IFN) responses. The antiviral function of IFN is mainly exerted by activating the JAK/STAT signalling and subsequently inducing IFN-stimulated gene (ISG) production. However, the mechanism by which IAV combat the type I IFN signalling pathway is not fully elucidated. In this study, we explored the roles of human microRNAs modulated by IAV infection in type I IFN responses. We demonstrated that microRNA-30 (miR-30) family members were downregulated by IAV infection. Our data showed that the forced expression of miR-30 family members inhibited IAV proliferation, while miR-30 family member inhibitors promoted IAV proliferation. Mechanistically, we found that miR-30 family members targeted and reduced SOCS1 and SOCS3 expression, and thus relieved their inhibiting effects on IFN/JAK/STAT signalling pathway. In addition, miR-30 family members inhibited the expression of NEDD4, a negative regulator of IFITM3, which is important for host defence against influenza viruses. Our findings suggest that IAV utilises a novel strategy to restrain host type I IFN-mediated antiviral immune responses by decreasing the expression of miR-30 family members, and add a new way to understand the mechanism of immune escape caused by influenza viruses. |A549 Cells [MESH] |Down-Regulation [MESH] |HeLa Cells [MESH] |Host-Pathogen Interactions/immunology [MESH] |Humans [MESH] |Influenza A virus/*drug effects/genetics [MESH] |Influenza, Human/*drug therapy [MESH] |MicroRNAs/genetics/*pharmacology [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |RNA-Binding Proteins/genetics/*metabolism [MESH] |Suppressor of Cytokine Signaling 1 Protein/genetics/*metabolism [MESH]Human microRNA-30 inhibits influenza virus infection by suppressing th(epmc).pdf DeepDyve Pubget Overpricing