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Details on Person Accessory open reading frame protein 6 (ORF6 or 6) of severe...
| Class:Id | Summation:9705279 |
|---|---|
| _displayName | Accessory open reading frame protein 6 (ORF6 or 6) of severe... |
| _timestamp | 2022-02-18 05:08:25 |
| created | [InstanceEdit:9705291] Shamovsky, Veronica, 2020-10-22 |
| literatureReference | [LiteratureReference:9705074] Evasion of Type I Interferon by SARS-CoV-2 [LiteratureReference:9705295] SARS-CoV-2 nsp13, nsp14, nsp15 and orf6 function as potent interferon antagonists [LiteratureReference:9705298] Severe acute respiratory syndrome coronavirus ORF6 antagonizes STAT1 function by sequestering nuclear import factors on the rough endoplasmic reticulum/Golgi membrane [LiteratureReference:9705294] Severe acute respiratory syndrome coronavirus open reading frame (ORF) 3b, ORF 6, and nucleocapsid proteins function as interferon antagonists [LiteratureReference:9705280] The ORF6, ORF8 and nucleocapsid proteins of SARS-CoV-2 inhibit type I interferon signaling pathway [LiteratureReference:9717695] Activation and evasion of type I interferon responses by SARS-CoV-2 |
| modified | [InstanceEdit:9708883] Shamovsky, Veronica, 2020-12-03 [InstanceEdit:9717699] Shamovsky, Veronica, 2021-03-13 [InstanceEdit:9756267] Shamovsky, Veronica, 2021-10-12 [InstanceEdit:9757471] Shamovsky, Veronica, 2021-11-01 [InstanceEdit:9760734] Shamovsky, Veronica, 2021-12-24 [InstanceEdit:9766213] Shamovsky, Veronica, 2022-02-18 |
| text | Accessory open reading frame protein 6 (ORF6 or 6) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exhibited strong inhibition on type I interferon (IFN)-responsive promoter activation in human embryonic kidney 293 (HEK293) cells that were transfected with luciferase reporter plasmid pIFN-β-luc and viral protein expressing plasmid (Li JY et al. 2020; Yuen CK et al. 2020; Xia H et al. 2020; Lei X et al. 2020). Fluorescence microscopy revealed that the overexpression of viral 6 (ORF6) protein blocked translocation of interferon regulatory factor 3 (IRF3) to the cell nucleus in poly(I:C)-induced human alveolar basal epithelial A549 cells (Xia H et al. 2020) and in Sendai virus (SeV)-induced HEK293T cells (Lei X et al. 2020). Mutagenesis analysis showed that the C-terminus of SARS-CoV-2 6 (from a.a. 53 to 61) is responsible for its antagonistic activity (Lei X et al. 2020). Co-immunoprecipitation using HEK293 cells that were co-transfected with FLAG-tagged ORF6-expressing plasmid and HA-tagged karyopherin α 1–6 (KPNA1–6) plasmids showed that viral ORF6 selectively interacted with KPNA2 but not the other KPNAs, suggesting that ORF6 inhibits IFN-β production by binding to KPNA2 to block IRF3 nuclear translocation (Xia H et al. 2020). Moreover, overexpression of viral ORF6 blocked STAT1 nuclear translocation in HEK293T cells (Lei X et al. 2020). Similar findings were reported for SARS-CoV-1 6 (ORF6) which inhibited IRFs-mediated IFN production (Kopecky-Bromberg SA et al. 2007) and antagonized STAT1 function (IFN signaling) by tethering the nuclear import factors KPNA2 and KPNB1 to the ER/Golgi membrane (Frieman M et al. 2007). These data suggest that SARS-CoV 6 antagonizes both production and signaling of type I IFNs by preventing nuclear translocation of transcription factors. This Reactome event describes binding of SARS-CoV-2 6 to KPNA2. |
| (summation) | [Reaction:9705299] SARS-CoV-2 6 binds KPNA2 [Homo sapiens] |
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No pathways have been reviewed or authored by Accessory open reading frame protein 6 (ORF6 or 6) of severe... (9705279)
