ArticleNature cell biology2004
Phosphorylation of the enteropathogenic E. coli receptor by the Src-family kinase c-Fyn triggers actin pedestal formation.
Article in Nature cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
51 citing papers in PubMed, 121 citations in OpenAlex.
- GBP1 recruitment to actin-rich pedestals of extracellular Gram-negative bacteria promotes pyroptosis.The EMBO journal · 2026Article
- GBP1 recruitment to actin-rich pedestals induced by extracellular Gram negative bacteria promotes pyroptosis.bioRxiv : the preprint server for biology · 2025Article
- Cytoskeletal mechanisms regulating attaching/effacing bacteria interactions with host cells: It takes a village to build the pedestal.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Modulating Liquid-Liquid Phase Separation of Nck Adaptor Protein against EnteropathogenicACS central science · 2023Article
- Using Linear Motif Database Resources to Identify SH2 Domain Binders.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Review
- Staying out or Going in? The Interplay between Type 3 and Type 5 Secretion Systems in Adhesion and Invasion of Enterobacterial Pathogens.International journal of molecular sciences · 2020Review
- EnteropathogenicInternational journal of molecular sciences · 2020Article
- Endocytosis and the internalization of pathogenic organisms: focus on phosphoinositides.F1000Research · 2020Review
- Coordinated transient interaction of ZO-1 and afadin is required for pedestal maturation induced by EspF from enteropathogenic Escherichia coli.MicrobiologyOpen · 2019Article
- Article
- Enteropathogenic E. coli relies on collaboration between the formin mDia1 and the Arp2/3 complex for actin pedestal biogenesis and maintenance.PLoS pathogens · 2018Article
- Extracellular motility and cell-to-cell transmission of enterohemorrhagic E. coli is driven by EspFU-mediated actin assembly.PLoS pathogens · 2017Article
- Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins.Cellular & molecular immunology · 2017Review
- Modification of Bacterial Effector Proteins Inside Eukaryotic Host Cells.Frontiers in cellular and infection microbiology · 2016Review
- Tir Is Essential for the Recruitment of Tks5 to Enteropathogenic Escherichia coli Pedestals.PloS one · 2015Article
- The Escherichia coli effector EspJ blocks Src kinase activity via amidation and ADP ribosylation.Nature communications · 2014Article
- The ability of an attaching and effacing pathogen to trigger localized actin assembly contributes to virulence by promoting mucosal attachment.Cellular microbiology · 2014Article
- Actin pedestal formation by enterohemorrhagic Escherichia coli enhances bacterial host cell attachment and concomitant type III translocation.Infection and immunity · 2014Article
- Indispensable functions of ABL and PDGF receptor kinases in epithelial adherence of attaching/effacing pathogens under physiological conditions.American journal of physiology. Cell physiology · 2014Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enteropathogenic Escherichia coli (EPEC) causes diarrhoeal disease worldwide. Pathogen adherence to host cells induces reorganization of the actin cytoskeleton into 'pedestal-like' pseudopods beneath the extracellular bacteria. This requires two bacterial virulence factors that mimic a ligand-receptor interaction. EPEC delivers its own receptor, the translocated intimin receptor (Tir), into the target cell plasma membrane, which is phosphorylated on interaction with the bacterial surface protein intimin. Tir phosphorylated on Tyr 474 (ref. 4) binds the cellular adaptor Nck, triggering actin polymerization. Nevertheless, despite its critical role, the mechanism of Tir Tyr 474 phosphorylation remains unknown. Here, by artificially uncoupling Tir delivery and activity, we show that Tir phosphorylation and Nck-dependent pedestal formation require the Src-family kinase (SFK) c-Fyn. SFK inhibitors prevent Tyr 474 phosphorylation, and cells lacking c-fyn are resistant to pedestal formation. c-Fyn exclusively phosphorylates clustered Tir in vitro, and kinase knockdown suppresses Tir phosphorylation and pedestal formation in cultured cells. These results identify the transient interaction with host c-Fyn as a pivotal link between bacterial Tir and the cellular Nck-WASP-Arp2/3 cascade, illuminating a tractable experimental system in which to dissect tyrosine kinase signalling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.