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10.1073/pnas.1322118111

http://scihub22266oqcxt.onion/10.1073/pnas.1322118111
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suck abstract from ncbi


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pmid24799673      Proc+Natl+Acad+Sci+U+S+A 2014 ; 111 (20): E2110-9
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  • NLRX1 prevents mitochondrial induced apoptosis and enhances macrophage antiviral immunity by interacting with influenza virus PB1-F2 protein #MMPMID24799673
  • Jaworska J; Coulombe F; Downey J; Tzelepis F; Shalaby K; Tattoli I; Berube J; Rousseau S; Martin JG; Girardin SE; McCullers JA; Divangahi M
  • Proc Natl Acad Sci U S A 2014[May]; 111 (20): E2110-9 PMID24799673show ga
  • Apoptosis refers to the ability of a cell to undergo programmed cell death under normal physiological conditions or in response to stress signals. During infection, influenza A viruses have the capacity to induce early apoptosis of immune cells, thereby preventing them from performing their antiviral function. In this study, we identified that a host innate immune sensor [NLRX1 (nucleotide-binding oligomerization domain-like receptor X1)] has the capacity to bind a small death-inducing protein from influenza A virus [PB1-F2 (polymerase basic protein 1-frame 2)] and defend immune cells against virus-driven apoptosis. This phenomenon allows the immune cells to survive longer and effectively restrict viral replication, protecting the host against the detrimental consequences of influenza.
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