Gasdermin B in the host-pathogen tug-of-war
The Shigella flexneri effector IpaH7.8 targets gasdermin B for degradation in infected host cells.This bacterial strategy counteracts a host defense mechanism in which the lymphoid cell compartment activates the bactericidal properties of gasdermin B.
It is well appreciated that host cells are not the only beneficiaries of protein post-translational modifications (PTMs).Large-scale quantitative proteomic studies demonstrated that various bacterial pathogens modulate specific host signaling pathways via inducing PTMs.Notable recent examples include the modulation of actin polymerization machinery by Salmonella enterica,1 autophagy receptors by Mycobacterium tuberculosis2 or innate immunity mechanisms by Shigella flexneri (S.flexneri),3 among other studies.
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2021-11-11(万方平台首次上网日期,不代表论文的发表时间)
共2页
1043-1044