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10.1016/j.celrep.2021.108761 http://scihub22266oqcxt.onion/10.1016/j.celrep.2021.108761 33567255!7857071!33567255     free     free     free 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       Cell+Rep 2021 ; 34 (7): 108761 Nephropedia Template TP {{tp|p=33567255|t=2021. SARS-CoV-2 ORF9b inhibits RIG-I-MAVS antiviral signaling by interrupting K63-linked ubiquitination of NEMO |pdf=|usr=}}{{33567255}} gab.com Text SARS-CoV-2 ORF9b inhibits RIG-I-MAVS antiviral signaling by interrupting K63-linked ubiquitination of NEMO JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33567255 #FOAvip Coronavirus disease 2019 (COVID-19) is a current global health threat caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Emerging evidence indicates that SARS-CoV-2 elicits a dysregulated immune response and a delayed interferon (IFN) expression in patients, which contribute largely to the viral pathogenesis and development of COVID-19. However, underlying mechanisms remain to be elucidated. Here, we report the activation and repression of the innate immune response by SARS-CoV-2. We show that SARS-CoV-2 RNA activates the RIG-I-MAVS-dependent IFN signaling pathway. We further uncover that ORF9b immediately accumulates and antagonizes the antiviral type I IFN response during SARS-CoV-2 infection on primary human pulmonary alveolar epithelial cells. ORF9b targets the nuclear factor kappaB (NF-kappaB) essential modulator NEMO and interrupts its K63-linked polyubiquitination upon viral stimulation, thereby inhibiting the canonical IkappaB kinase alpha (IKKalpha)/beta/gamma-NF-kappaB signaling and subsequent IFN production. Our findings thus unveil the innate immunosuppression by ORF9b and provide insights into the host-virus interplay during the early stage of SARS-CoV-2 infection. Twit Text FOAVip SARS-CoV-2 ORF9b inhibits RIG-I-MAVS antiviral signaling by interrupting K63-linked ubiquitination of NEMO ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33567255 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33567255 #FOAvip English Wikipedia <ref>{{Cite pmid|33567255}}</ref> SARS-CoV-2 ORF9b inhibits RIG-I-MAVS antiviral signaling by interrupting K63-linked ubiquitination of NEMO #MMPMID33567255 Wu J; Shi Y; Pan X; Wu S; Hou R; Zhang Y; Zhong T; Tang H; Du W; Wang L; Wo J; Mu J; Qiu Y; Yang K; Zhang LK; Ye BC; Qi N Cell Rep 2021[Feb]; 34 (7): 108761 PMID33567255show ga Coronavirus disease 2019 (COVID-19) is a current global health threat caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Emerging evidence indicates that SARS-CoV-2 elicits a dysregulated immune response and a delayed interferon (IFN) expression in patients, which contribute largely to the viral pathogenesis and development of COVID-19. However, underlying mechanisms remain to be elucidated. Here, we report the activation and repression of the innate immune response by SARS-CoV-2. We show that SARS-CoV-2 RNA activates the RIG-I-MAVS-dependent IFN signaling pathway. We further uncover that ORF9b immediately accumulates and antagonizes the antiviral type I IFN response during SARS-CoV-2 infection on primary human pulmonary alveolar epithelial cells. ORF9b targets the nuclear factor kappaB (NF-kappaB) essential modulator NEMO and interrupts its K63-linked polyubiquitination upon viral stimulation, thereby inhibiting the canonical IkappaB kinase alpha (IKKalpha)/beta/gamma-NF-kappaB signaling and subsequent IFN production. Our findings thus unveil the innate immunosuppression by ORF9b and provide insights into the host-virus interplay during the early stage of SARS-CoV-2 infection. |Adaptor Proteins, Signal Transducing/metabolism[MESH] |Alveolar Epithelial Cells/metabolism/virology[MESH] |COVID-19/immunology/metabolism[MESH] |Coronavirus Nucleocapsid Proteins/*genetics/metabolism[MESH] |HEK293 Cells[MESH] |Humans[MESH] |I-kappa B Kinase/*metabolism[MESH] |Immunity, Innate/immunology[MESH] |Interferon Type I/metabolism[MESH] |Interferons/metabolism[MESH] |NF-kappa B/metabolism[MESH] |Phosphoproteins/genetics/metabolism[MESH] |Primary Cell Culture[MESH] |Receptors, Retinoic Acid/metabolism[MESH] |SARS-CoV-2/genetics/immunology/*metabolism[MESH] |Signal Transduction[MESH]SARS-CoV-2 ORF9b inhibits RIG-I-MAVS antiviral signaling by interrupti(epmc).pdf DeepDyve Pubget Overpricing