Matches in SemOpenAlex for { <https://semopenalex.org/work/W3041706475> ?p ?o ?g. }
- W3041706475 abstract "Upon invasive bacterial infection of colonic epithelium, host cells induce several types of death to eliminate pathogens. For instance, necroptosis is a RIPK-dependent lytic death that serves as a backup system to fully eliminate intracellular pathogens when apoptosis is inhibited; this phenomenon has been termed cell death crosstalk. To maintain their replicative niche and multiply within cells, some enteric pathogens prevent epithelial death by delivering effectors via the type III secretion system. In this study, we found that Shigella hijacks host death crosstalk via a dual mechanism: inhibition of apoptosis by the OspC1 effector and inhibition of necroptosis by the OspD3 effector. Upon infection by Shigella, host cells recognize blockade of caspase-8 apoptosis signaling by OspC1 effector as a key danger signal and trigger necroptosis as a backup form of host defense. To counteract this backup defense, Shigella delivers the OspD3 effector, a protease, to degrade RIPK1 and RIPK3, preventing necroptosis. We believe that blockade of host death crosstalk by Shigella is a unique intracellular survival tactic for prolonging the bacterium's replicative niche." @default.
- W3041706475 created "2020-07-16" @default.
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- W3041706475 date "2020-07-13" @default.
- W3041706475 modified "2023-10-18" @default.
- W3041706475 title "A unique bacterial tactic to circumvent the cell death crosstalk induced by blockade of caspase‐8" @default.
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- W3041706475 doi "https://doi.org/10.15252/embj.2020104469" @default.
- W3041706475 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7459423" @default.
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