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  • SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules #MMPMID35075101
  • Zheng Y; Deng J; Han L; Zhuang MW; Xu Y; Zhang J; Nan ML; Xiao Y; Zhan P; Liu X; Gao C; Wang PH
  • Signal Transduct Target Ther 2022[Jan]; 7 (1): 22 PMID35075101show ga
  • As a highly pathogenic human coronavirus, SARS-CoV-2 has to counteract an intricate network of antiviral host responses to establish infection and spread. The nucleic acid-induced stress response is an essential component of antiviral defense and is closely related to antiviral innate immunity. However, whether SARS-CoV-2 regulates the stress response pathway to achieve immune evasion remains elusive. In this study, SARS-CoV-2 NSP5 and N protein were found to attenuate antiviral stress granule (avSG) formation. Moreover, NSP5 and N suppressed IFN expression induced by infection of Sendai virus or transfection of a synthetic mimic of dsRNA, poly (I:C), inhibiting TBK1 and IRF3 phosphorylation, and restraining the nuclear translocalization of IRF3. Furthermore, HEK293T cells with ectopic expression of NSP5 or N protein were less resistant to vesicular stomatitis virus infection. Mechanistically, NSP5 suppressed avSG formation and disrupted RIG-I-MAVS complex to attenuate the RIG-I-mediated antiviral immunity. In contrast to the multiple targets of NSP5, the N protein specifically targeted cofactors upstream of RIG-I. The N protein interacted with G3BP1 to prevent avSG formation and to keep the cofactors G3BP1 and PACT from activating RIG-I. Additionally, the N protein also affected the recognition of dsRNA by RIG-I. This study revealed the intimate correlation between SARS-CoV-2, the stress response, and innate antiviral immunity, shedding light on the pathogenic mechanism of COVID-19.
  • |Animals[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Coronavirus 3C Proteases/*genetics/immunology[MESH]
  • |Coronavirus Nucleocapsid Proteins/*genetics/immunology[MESH]
  • |DEAD Box Protein 58/*genetics/immunology[MESH]
  • |DNA Helicases/*genetics/immunology[MESH]
  • |Gene Expression Regulation[MESH]
  • |HEK293 Cells[MESH]
  • |HeLa Cells[MESH]
  • |Humans[MESH]
  • |Immune Evasion[MESH]
  • |Phosphoproteins/genetics/immunology[MESH]
  • |Poly I-C/pharmacology[MESH]
  • |Poly-ADP-Ribose Binding Proteins/*genetics/immunology[MESH]
  • |Protein Binding[MESH]
  • |RNA Helicases/*genetics/immunology[MESH]
  • |RNA Recognition Motif Proteins/*genetics/immunology[MESH]
  • |RNA, Double-Stranded/genetics/immunology[MESH]
  • |RNA-Binding Proteins/*genetics/immunology[MESH]
  • |Receptors, Immunologic/*genetics/immunology[MESH]
  • |SARS-CoV-2/*genetics/immunology/pathogenicity[MESH]
  • |Sendai virus/genetics/immunology[MESH]
  • |Signal Transduction[MESH]
  • |Stress Granules/drug effects/*genetics/immunology/virology[MESH]
  • |Vero Cells[MESH]
  • |Vesiculovirus/genetics/immunology[MESH]

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  • suck abstract from ncbi

    22 1.7 2022