研究β2糖蛋白I(β2GPI)与肝细胞相互作用的过程,以进一步探讨β2GPI在乙型肝炎病毒感染肝细胞过程中所发挥的作用。采用L igand b lot技术,从SMMC-7721、HL-60及SGC-7901三个细胞株中,筛选出具有与人β2GPI特异结合蛋白成分的细胞。SMM...研究β2糖蛋白I(β2GPI)与肝细胞相互作用的过程,以进一步探讨β2GPI在乙型肝炎病毒感染肝细胞过程中所发挥的作用。采用L igand b lot技术,从SMMC-7721、HL-60及SGC-7901三个细胞株中,筛选出具有与人β2GPI特异结合蛋白成分的细胞。SMMC-7721细胞在40kD处出现一特异染色带,而HL-60及SGC-7901二种细胞则无此反应。在SMMC-7721细胞中存在有与人β2GPI特异结合的蛋白,这种蛋白可能参与了HBV感染肝细胞的过程。展开更多
A novel SARS-related coronavirus(SARS-CoV-2)has recently emerged as a serious pathogen that causes high morbidity and substantial mortality.However,the mechanisms by which SARS-CoV-2 evades host immunity remain poorly...A novel SARS-related coronavirus(SARS-CoV-2)has recently emerged as a serious pathogen that causes high morbidity and substantial mortality.However,the mechanisms by which SARS-CoV-2 evades host immunity remain poorly understood.Here,we identified SARS-CoV-2 membrane glycoprotein M as a negative regulator of the innate immune response.We found that the M protein interacted with the central adaptor protein MAVS in the innate immune response pathways.This interaction impaired MAVS aggregation and its recruitment of downstream TRAF3,TBK1,and IRF3,leading to attenuation of the innate antiviral response.Our findings reveal a mechanism by which SARS-CoV-2 evades the innate immune response and suggest that the M protein of SARSCoV-2 is a potential target for the development of SARS-CoV-2 interventions.展开更多
文摘研究β2糖蛋白I(β2GPI)与肝细胞相互作用的过程,以进一步探讨β2GPI在乙型肝炎病毒感染肝细胞过程中所发挥的作用。采用L igand b lot技术,从SMMC-7721、HL-60及SGC-7901三个细胞株中,筛选出具有与人β2GPI特异结合蛋白成分的细胞。SMMC-7721细胞在40kD处出现一特异染色带,而HL-60及SGC-7901二种细胞则无此反应。在SMMC-7721细胞中存在有与人β2GPI特异结合的蛋白,这种蛋白可能参与了HBV感染肝细胞的过程。
基金supported by the National Key Research and Development Project of China(2020YFC0841000)the Strategic Priority Research Program(XDB29010302)+2 种基金the National Natural Science Foundation of China(31800732)the Key Research Programs of Frontier Sciences funded by the Chinese Academy of Sciencesthe Special Research Assistant Grant Program of the Chinese Academy of Sciences.
文摘A novel SARS-related coronavirus(SARS-CoV-2)has recently emerged as a serious pathogen that causes high morbidity and substantial mortality.However,the mechanisms by which SARS-CoV-2 evades host immunity remain poorly understood.Here,we identified SARS-CoV-2 membrane glycoprotein M as a negative regulator of the innate immune response.We found that the M protein interacted with the central adaptor protein MAVS in the innate immune response pathways.This interaction impaired MAVS aggregation and its recruitment of downstream TRAF3,TBK1,and IRF3,leading to attenuation of the innate antiviral response.Our findings reveal a mechanism by which SARS-CoV-2 evades the innate immune response and suggest that the M protein of SARSCoV-2 is a potential target for the development of SARS-CoV-2 interventions.
