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10.4049/jimmunol.2100684 http://scihub22266oqcxt.onion/10.4049/jimmunol.2100684 34996837!ä!34996837 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2022 ; 208 (3): 753-761 Nephropedia Template TP {{tp|p=34996837|t=2022. SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1 via p62-Dependent Selective Autophagy |pdf=|usr=}}{{34996837}} gab.com Text SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1 via p62-Dependent Selective Autophagy JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34996837 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has seriously threatened global public health. Severe COVID-19 has been reported to be associated with an impaired IFN response. However, the mechanisms of how SARS-CoV-2 antagonizes the host IFN response are poorly understood. In this study, we report that SARS-CoV-2 helicase NSP13 inhibits type I IFN production by directly targeting TANK-binding kinase 1 (TBK1) for degradation. Interestingly, inhibition of autophagy by genetic knockout of Beclin1 or pharmacological inhibition can rescue NSP13-mediated TBK1 degradation in HEK-293T cells. Subsequent studies revealed that NSP13 recruits TBK1 to p62, and the absence of p62 can also inhibit TBK1 degradation in HEK-293T and HeLa cells. Finally, TBK1 and p62 degradation and p62 aggregation were observed during SARS-CoV-2 infection in HeLa-ACE2 and Calu3 cells. Overall, our study shows that NSP13 inhibits type I IFN production by recruiting TBK1 to p62 for autophagic degradation, enabling it to evade the host innate immune response, which provides new insights into the transmission and pathogenesis of SARS-CoV-2 infection. Twit Text FOAVip SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1 via p62-Dependent Selective Autophagy ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34996837 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34996837 #FOAvip English Wikipedia <ref>{{Cite pmid|34996837}}</ref> SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1 via p62-Dependent Selective Autophagy #MMPMID34996837 Sui C; Xiao T; Zhang S; Zeng H; Zheng Y; Liu B; Xu G; Gao C; Zhang Z J Immunol 2022[Feb]; 208 (3): 753-761 PMID34996837show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has seriously threatened global public health. Severe COVID-19 has been reported to be associated with an impaired IFN response. However, the mechanisms of how SARS-CoV-2 antagonizes the host IFN response are poorly understood. In this study, we report that SARS-CoV-2 helicase NSP13 inhibits type I IFN production by directly targeting TANK-binding kinase 1 (TBK1) for degradation. Interestingly, inhibition of autophagy by genetic knockout of Beclin1 or pharmacological inhibition can rescue NSP13-mediated TBK1 degradation in HEK-293T cells. Subsequent studies revealed that NSP13 recruits TBK1 to p62, and the absence of p62 can also inhibit TBK1 degradation in HEK-293T and HeLa cells. Finally, TBK1 and p62 degradation and p62 aggregation were observed during SARS-CoV-2 infection in HeLa-ACE2 and Calu3 cells. Overall, our study shows that NSP13 inhibits type I IFN production by recruiting TBK1 to p62 for autophagic degradation, enabling it to evade the host innate immune response, which provides new insights into the transmission and pathogenesis of SARS-CoV-2 infection. |*Autophagy[MESH] |Beclin-1/antagonists & inhibitors[MESH] |COVID-19/*immunology[MESH] |Cell Line[MESH] |Coronavirus RNA-Dependent RNA Polymerase/*physiology[MESH] |Down-Regulation[MESH] |Humans[MESH] |Immune Evasion[MESH] |Immunity, Innate[MESH] |Immunoprecipitation[MESH] |Interferon Type I/*biosynthesis/genetics[MESH] |Methyltransferases/*physiology[MESH] |Multiprotein Complexes[MESH] |Protein Aggregates[MESH] |Protein Interaction Mapping[MESH] |Protein Serine-Threonine Kinases/*metabolism[MESH] |RNA Helicases/*physiology[MESH] |SARS-CoV-2/*physiology[MESH] |Sequestosome-1 Protein/*metabolism[MESH]SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1(epmc).pdf DeepDyve Pubget Overpricing