Journal article
Distinct roles of the antiapoptotic effectors NleB and NleF from enteropathogenic Escherichia coli
GL Pollock, CVL Oates, C Giogha, TWF Lung, SY Ong, JS Pearson, EL Hartland
Infection and Immunity | AMER SOC MICROBIOLOGY | Published : 2017
DOI: 10.1128/IAI.01071-16
Abstract
During infection, enteropathogenic Escherichia coli (EPEC) translocates effector proteins directly into the cytosol of infected enterocytes using a type III secretion system (T3SS). Once inside the host cell, these effector proteins subvert various immune signaling pathways, including death receptor-induced apoptosis. One such effector protein is the non-locus of enterocyte effacement (LEE)-encoded effector NleB1, which inhibits extrinsic apoptotic signaling via the FAS death receptor. NleB1 transfers a single N-acetylglucosamine (GlcNAc) residue to Arg117 in the death domain of Fas-associated protein with death domain (FADD) and inhibits FAS ligand (FasL)-stimulated caspase-8 cleavage. Anot..
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Awarded by Australian National Health and Medical Research Council
Awarded by Early Career Fellowship
Funding Acknowledgements
This work was supported by the Australian National Health and Medical Research Council (project grants APP1098826 and APP1044061 to E. L. H. and Early Career Fellowship APP1090108 to J.S.P.). G.L.P. and C.G. were supported by Australian postgraduate awards. T.W.F.L. was supported by a University of Melbourne International Research Scholarship (MIRS).