During virus infection,RIG-I-like receptors(RLRs)recognize viral RNAs and recruit the adaptor protein VISA to activate downstream signaling,leading to activation of transcription factors NF-κB and IRF3,which collabor...During virus infection,RIG-I-like receptors(RLRs)recognize viral RNAs and recruit the adaptor protein VISA to activate downstream signaling,leading to activation of transcription factors NF-κB and IRF3,which collaborate to induce type I interferons(IFNs).IFNs further induce expression of hundreds of IFN-stimulated genes(ISGs)that suppress viral replication and facilitate the adaptive immune response.Dysregulated production of IFNs is implicated in various immune diseases.Here we identified Signal Recognition Particle 54(SRP54)as a negative regulator of RLRs-induced antiviral signaling.Overexpression of SRP54 inhibited RNA virus-triggered induction of IFN-b and increased viral replication,whereas knockdown of SRP54 had opposite effects.Mechanistically,SRP54 interacted with both RIG-I and MDA5 and impaired their association with VISA.Our findings demonstrate that SRP54 acts as a negative regulator of RLRs-mediated innate immune response by disrupting the recruitment of VISA to RIG-I/MDA5.展开更多
Dear Editor,In December 2019,a novel coronavirus that is related to severe acute respiratory syndrome coronavirus(SARS-CoV)and Middle East respiratory syndrome coronavirus(MERS-CoV)in phylogenetic distance was identif...Dear Editor,In December 2019,a novel coronavirus that is related to severe acute respiratory syndrome coronavirus(SARS-CoV)and Middle East respiratory syndrome coronavirus(MERS-CoV)in phylogenetic distance was identified.1 This virus,which was later designated as SARS-CoV-2,also causes acute respiratory disease syndrome(ARDS)termed coronavirus disease 2019(COVID-19),which was declared as a pandemic by the World Health Organization in March 2020.展开更多
基金supported by the National Natural Science Foundation of China(31770946,awarded to Y.Y.)Key Research Programs of Frontier Science(awarded to Y.Y.W.)funded by Chinese Academy of Sciences。
文摘During virus infection,RIG-I-like receptors(RLRs)recognize viral RNAs and recruit the adaptor protein VISA to activate downstream signaling,leading to activation of transcription factors NF-κB and IRF3,which collaborate to induce type I interferons(IFNs).IFNs further induce expression of hundreds of IFN-stimulated genes(ISGs)that suppress viral replication and facilitate the adaptive immune response.Dysregulated production of IFNs is implicated in various immune diseases.Here we identified Signal Recognition Particle 54(SRP54)as a negative regulator of RLRs-induced antiviral signaling.Overexpression of SRP54 inhibited RNA virus-triggered induction of IFN-b and increased viral replication,whereas knockdown of SRP54 had opposite effects.Mechanistically,SRP54 interacted with both RIG-I and MDA5 and impaired their association with VISA.Our findings demonstrate that SRP54 acts as a negative regulator of RLRs-mediated innate immune response by disrupting the recruitment of VISA to RIG-I/MDA5.
基金supported by the CAS Pilot Project(XDB29010302)National Natural Science Foundation of China(31700758)+1 种基金the CAS Emergency Project for COVID-19 Prevention and Control(2020JFK0100)the CAS Key Research Programs of Frontier Sciences.
文摘Dear Editor,In December 2019,a novel coronavirus that is related to severe acute respiratory syndrome coronavirus(SARS-CoV)and Middle East respiratory syndrome coronavirus(MERS-CoV)in phylogenetic distance was identified.1 This virus,which was later designated as SARS-CoV-2,also causes acute respiratory disease syndrome(ARDS)termed coronavirus disease 2019(COVID-19),which was declared as a pandemic by the World Health Organization in March 2020.
