Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


suck pdf from google scholar
unlimited free pdf from europmc34845370    free
PDF from PMC    free
html from PMC    free
PDF vom PMID34845370  :  Publisher

suck abstract from ncbi

Nephropedia Template TP Text

Twit Text FOAVip

Twit Text #

English Wikipedia

  • SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy #MMPMID34845370
  • Li X; Hou P; Ma W; Wang X; Wang H; Yu Z; Chang H; Wang T; Jin S; Wang X; Wang W; Zhao Y; Zhao Y; Xu C; Ma X; Gao Y; He H
  • Cell Mol Immunol 2022[Jan]; 19 (1): 67-78 PMID34845370show ga
  • The global coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused severe morbidity and mortality in humans. It is urgent to understand the function of viral genes. However, the function of open reading frame 10 (ORF10), which is uniquely expressed by SARS-CoV-2, remains unclear. In this study, we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon (IFN-I) genes and IFN-stimulated genes. Then, mitochondrial antiviral signaling protein (MAVS) was identified as the target via which ORF10 suppresses the IFN-I signaling pathway, and MAVS was found to be degraded through the ORF10-induced autophagy pathway. Furthermore, overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy. Mechanistically, ORF10 was translocated to mitochondria by interacting with the mitophagy receptor Nip3-like protein X (NIX) and induced mitophagy through its interaction with both NIX and LC3B. Moreover, knockdown of NIX expression blocked mitophagy activation, MAVS degradation, and IFN-I signaling pathway inhibition by ORF10. Consistent with our observations, in the context of SARS-CoV-2 infection, ORF10 inhibited MAVS expression and facilitated viral replication. In brief, our results reveal a novel mechanism by which SARS-CoV-2 inhibits the innate immune response; that is, ORF10 induces mitophagy-mediated MAVS degradation by binding to NIX.
  • |*Open Reading Frames[MESH]
  • |*Signal Transduction[MESH]
  • |Adaptor Proteins, Signal Transducing/metabolism[MESH]
  • |Antiviral Agents/metabolism[MESH]
  • |Autophagy/immunology[MESH]
  • |COVID-19/*genetics/*virology[MESH]
  • |Gene Silencing[MESH]
  • |HEK293 Cells[MESH]
  • |HeLa Cells[MESH]
  • |Humans[MESH]
  • |Immunity, Innate/*immunology[MESH]
  • |Interferon Type I/metabolism[MESH]
  • |Mitochondria/metabolism[MESH]
  • |Mitophagy[MESH]
  • |Proteasome Endopeptidase Complex/metabolism[MESH]
  • |SARS-CoV-2/*genetics[MESH]
  • |Ubiquitination[MESH]
  • |Viral Proteins/metabolism[MESH]
  • |Virus Replication[MESH]

  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    67 1.19 2022