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10.1038/s41423-020-00619-y http://scihub22266oqcxt.onion/10.1038/s41423-020-00619-y 33637958!7907794!33637958     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Immunol 2021 ; 18 (4): 945-953 Nephropedia Template TP {{tp|p=33637958|t=2021. SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation |pdf=|usr=}}{{33637958}} gab.com Text SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation JO: Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33637958 #FOAvip SARS-CoV-2 is the pathogenic agent of COVID-19, which has evolved into a global pandemic. Compared with some other respiratory RNA viruses, SARS-CoV-2 is a poor inducer of type I interferon (IFN). Here, we report that SARS-CoV-2 nsp12, the viral RNA-dependent RNA polymerase (RdRp), suppresses host antiviral responses. SARS-CoV-2 nsp12 attenuated Sendai virus (SeV)- or poly(I:C)-induced IFN-beta promoter activation in a dose-dependent manner. It also inhibited IFN promoter activation triggered by RIG-I, MDA5, MAVS, and IRF3 overexpression. Nsp12 did not impair IRF3 phosphorylation but suppressed the nuclear translocation of IRF3. Mutational analyses suggested that this suppression was not dependent on the polymerase activity of nsp12. Given these findings, our study reveals that SARS-CoV-2 RdRp can antagonize host antiviral innate immunity and thus provides insights into viral pathogenesis. Twit Text FOAVip SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation ????Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33637958 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33637958 #FOAvip English Wikipedia <ref>{{Cite pmid|33637958}}</ref> SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation #MMPMID33637958 Wang W; Zhou Z; Xiao X; Tian Z; Dong X; Wang C; Li L; Ren L; Lei X; Xiang Z; Wang J Cell Mol Immunol 2021[Apr]; 18 (4): 945-953 PMID33637958show ga SARS-CoV-2 is the pathogenic agent of COVID-19, which has evolved into a global pandemic. Compared with some other respiratory RNA viruses, SARS-CoV-2 is a poor inducer of type I interferon (IFN). Here, we report that SARS-CoV-2 nsp12, the viral RNA-dependent RNA polymerase (RdRp), suppresses host antiviral responses. SARS-CoV-2 nsp12 attenuated Sendai virus (SeV)- or poly(I:C)-induced IFN-beta promoter activation in a dose-dependent manner. It also inhibited IFN promoter activation triggered by RIG-I, MDA5, MAVS, and IRF3 overexpression. Nsp12 did not impair IRF3 phosphorylation but suppressed the nuclear translocation of IRF3. Mutational analyses suggested that this suppression was not dependent on the polymerase activity of nsp12. Given these findings, our study reveals that SARS-CoV-2 RdRp can antagonize host antiviral innate immunity and thus provides insights into viral pathogenesis. |Adaptor Proteins, Signal Transducing/genetics/metabolism[MESH] |COVID-19/*metabolism[MESH] |Cell Nucleus/metabolism[MESH] |Coronavirus RNA-Dependent RNA Polymerase/*metabolism[MESH] |DEAD Box Protein 58/genetics/metabolism[MESH] |Host-Pathogen Interactions/immunology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Interferon Regulatory Factor-3/genetics/*metabolism[MESH] |Interferon Type I/genetics/*metabolism[MESH] |Interferon-Induced Helicase, IFIH1/genetics/metabolism[MESH] |Interferon-beta/genetics/metabolism[MESH] |Mutation[MESH] |Phosphorylation[MESH] |Promoter Regions, Genetic[MESH] |Receptors, Immunologic/genetics/metabolism[MESH] |SARS-CoV-2/enzymology/*metabolism[MESH]SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting(epmc).pdf DeepDyve Pubget Overpricing