ArticleCellular microbiology2013
Myosin-X facilitates Shigella-induced membrane protrusions and cell-to-cell spread.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- A pore-forming toxin initiates ABI1 complex switching to promote bacterial cell-to-cell spread.Nature communications · 2026Article
- Pathogen-induced rerouting of host membrane trafficking.Current opinion in cell biology · 2025Review
- Host PIK3C3 promotes Shigella flexneri spread from cell to cell through vacuole formation.PLoS pathogens · 2025Article
- ThemBio · 2025Article
- Cells stably expressing shRNA against MYO10 display altered cell motility.microPublication biology · 2025Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- The type 3 secretion effector IpgD promotes S. flexneri dissemination.PLoS pathogens · 2022Article
- Imaging Cytoskeleton Components by Electron Microscopy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Myosins, an Underestimated Player in the Infectious Cycle of Pathogenic Bacteria.International journal of molecular sciences · 2021Review
- Principles of intracellular bacterial pathogen spread from cell to cell.PLoS pathogens · 2018Review
- Pathways of host cell exit by intracellular pathogens.Microbial cell (Graz, Austria) · 2018Review
- Myosin X is required for efficient melanoblast migration and melanoma initiation and metastasis.Scientific reports · 2018Article
- A Salutary Role of Reactive Oxygen Species in Intercellular Tunnel-Mediated Communication.Frontiers in cell and developmental biology · 2018Review
- Actin-based motility and cell-to-cell spread of bacterial pathogens.Current opinion in microbiology · 2017Review
- Transcriptional Categorization of the Etiology of Pneumonia Syndrome in Pediatric Patients in Malaria-Endemic Areas.The Journal of infectious diseases · 2017Article
- Cellular Aspects of Shigella Pathogenesis: Focus on the Manipulation of Host Cell Processes.Frontiers in cellular and infection microbiology · 2016Review
- Molecular and Cellular Mechanisms of Shigella flexneri Dissemination.Frontiers in cellular and infection microbiology · 2016Review
- Bacterial spread from cell to cell: beyond actin-based motility.Trends in microbiology · 2015Review
- Novel microscopy-based screening method reveals regulators of contact-dependent intercellular transfer.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The intracellular pathogen Shigella flexneri forms membrane protrusions to spread from cell to cell. As protrusions form, myosin-X (Myo10) localizes to Shigella. Electron micrographs of immunogold-labelled Shigella-infected HeLa cells reveal that Myo10 concentrates at the bases and along the sides of bacteria within membrane protrusions. Time-lapse video microscopy shows that a full-length Myo10 GFP-construct cycles along the sides of Shigella within the membrane protrusions as these structures progressively lengthen. RNAi knock-down of Myo10 is associated with shorter protrusions with thicker stalks, and causes a >80% decrease in confluent cell plaque formation. Myo10 also concentrates in membrane protrusions formed by another intracellular bacteria, Listeria, and knock-down of Myo10 also impairs Listeria plaque formation. In Cos7 cells (contain low concentrations of Myo10), the expression of full-length Myo10 nearly doubles Shigella-induced protrusion length, and lengthening requires the head domain, as well as the tail-PH domain, but not the FERM domain. The GFP-Myo10-HMM domain localizes to the sides of Shigella within membrane protrusions and the GFP-Myo10-PH domain localizes to host cell membranes. We conclude thatMyo10 generates the force to enhance bacterial-induced protrusions by binding its head region to actin filaments and its PH tail domain to the peripheral membrane.
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Registered trials
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.