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10.1038/s41423-021-00807-4 http://scihub22266oqcxt.onion/10.1038/s41423-021-00807-4 34845370!8628139!34845370     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 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Immunol 2022 ; 19 (1): 67-78 Nephropedia Template TP {{tp|p=34845370|t=2022. SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy |pdf=|usr=}}{{34845370}} gab.com Text SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy JO: Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34845370 #FOAvip The global coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused severe morbidity and mortality in humans. It is urgent to understand the function of viral genes. However, the function of open reading frame 10 (ORF10), which is uniquely expressed by SARS-CoV-2, remains unclear. In this study, we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon (IFN-I) genes and IFN-stimulated genes. Then, mitochondrial antiviral signaling protein (MAVS) was identified as the target via which ORF10 suppresses the IFN-I signaling pathway, and MAVS was found to be degraded through the ORF10-induced autophagy pathway. Furthermore, overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy. Mechanistically, ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X (NIX) and induced mitophagy through its interaction with both NIX and LC3B. Moreover, knockdown of NIX expression blocked mitophagy activation, MAVS degradation, and IFN-I signaling pathway inhibition by ORF10. Consistent with our observations, in the context of SARS-CoV-2 infection, ORF10 inhibited MAVS expression and facilitated viral replication. In brief, our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response; that is, ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX. Twit Text FOAVip SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy ????Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34845370 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34845370 #FOAvip English Wikipedia <ref>{{Cite pmid|34845370}}</ref> SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy #MMPMID34845370 Li X; Hou P; Ma W; Wang X; Wang H; Yu Z; Chang H; Wang T; Jin S; Wang X; Wang W; Zhao Y; Zhao Y; Xu C; Ma X; Gao Y; He H Cell Mol Immunol 2022[Jan]; 19 (1): 67-78 PMID34845370show ga The global coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused severe morbidity and mortality in humans. It is urgent to understand the function of viral genes. However, the function of open reading frame 10 (ORF10), which is uniquely expressed by SARS-CoV-2, remains unclear. In this study, we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon (IFN-I) genes and IFN-stimulated genes. Then, mitochondrial antiviral signaling protein (MAVS) was identified as the target via which ORF10 suppresses the IFN-I signaling pathway, and MAVS was found to be degraded through the ORF10-induced autophagy pathway. Furthermore, overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy. Mechanistically, ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X (NIX) and induced mitophagy through its interaction with both NIX and LC3B. Moreover, knockdown of NIX expression blocked mitophagy activation, MAVS degradation, and IFN-I signaling pathway inhibition by ORF10. Consistent with our observations, in the context of SARS-CoV-2 infection, ORF10 inhibited MAVS expression and facilitated viral replication. In brief, our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response; that is, ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX. |*Open Reading Frames[MESH] |*Signal Transduction[MESH] |Adaptor Proteins, Signal Transducing/metabolism[MESH] |Antiviral Agents/metabolism[MESH] |Autophagy/immunology[MESH] |COVID-19/*genetics/*virology[MESH] |Gene Silencing[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Humans[MESH] |Immunity, Innate/*immunology[MESH] |Interferon Type I/metabolism[MESH] |Mitochondria/metabolism[MESH] |Mitophagy[MESH] |Proteasome Endopeptidase Complex/metabolism[MESH] |SARS-CoV-2/*genetics[MESH] |Ubiquitination[MESH] |Viral Proteins/metabolism[MESH]SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by de(epmc).pdf DeepDyve Pubget Overpricing