Tyrosine kinase signaling and type III effectors orchestrating Shigella invasion
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Van Nhieu, GT
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Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, FranceInst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, France
Van Nhieu, GT
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Enninga, J
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Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, FranceInst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, France
Enninga, J
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Sansonetti, P
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Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, FranceInst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, France
Sansonetti, P
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Grompone, G
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Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, FranceInst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, France
Grompone, G
[1
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[1] Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris 15, France
Upon epithelial cell contact, Shigella type III effectors activate complex signaling pathways that induce localized membrane ruffling, resulting in Shigella invasion. Bacterial induced membrane ruffles require a timely coordination of cytoskeletal processes, including actin polymerization, filament reorganization and depolymerization, orchestrated by Rho GTPases and tyrosine kinases. An emerging concept is that multiple Shigella effectors act in synergy to promote actin polymerization in membrane extensions at the site of bacterial entry. Recent advances point to the role of AbI/Arg and Src tyrosine kinases as key regulators of bacterial induced cytoskeletal dynamics.