Evidence map›Paper›PMID 27311480›Full record

ArticleJournal of cell science2016

Staphylococcus aureus recruits Cdc42GAP through recycling endosomes and the exocyst to invade human endothelial cells.

Liane Rauch, Kirsten Hennings, Claudia Trasak, Anja Röder, Barbara Schröder, Friedrich Koch-Nolte, Felix Rivera-Molina, Derek Toomre, Martin Aepfelbacher

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  8. SNX27 suppresses SARS-CoV-2 infection by inhibiting viral lysosome/late endosome entry.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
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  12. Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Liane RauchInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany.
Kirsten HenningsInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany.
Claudia TrasakInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany.
Anja RöderInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany.
Barbara SchröderInstitute of Biological and Medical Imaging (IBMI), Helmholtz Zentrum München, Ingolstädter Landstraße 1, Neuherberg 85764, Germany Institute for Biological Imaging, Technical University of Munich, Arcisstrasse 21, Munich 80333, Germany.
Friedrich Koch-NolteInstitute of Immunology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany.
Felix Rivera-MolinaDepartment of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.
Derek ToomreDepartment of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.
Martin AepfelbacherInstitute of Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany m.aepfelbacher@uke.de.ORCID 0000-0003-2473-2970
Universität Hamburg · DEYale University · USHelmholtz Zentrum München · DE

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Dynamics of exocyst recruitment and assemblyR01GM098498 · NIGMS · YALE UNIVERSITY · PI TOOMRE, DEREK K. · 2013 to 2015
$1.0M
NIDDK NIH HHS P30 DK045735NIGMS NIH HHS R01 GM098498
6 · The paper itself

Abstract

Activation and invasion of the vascular endothelium by Staphylococcus aureus is a major cause of sepsis and endocarditis. For endothelial cell invasion, S. aureus triggers actin polymerization through Cdc42, N-WASp (also known as WASL) and the Arp2/3 complex to assemble a phagocytic cup-like structure. Here, we show that after stimulating actin polymerization staphylococci recruit Cdc42GAP (also known as ARHGAP1) which deactivates Cdc42 and terminates actin polymerization in the phagocytic cups. Cdc42GAP is delivered to the invading bacteria on recycling endocytic vesicles in concert with the exocyst complex. When Cdc42GAP recruitment by staphylococci was prevented by blocking recycling endocytic vesicles or the exocyst complex, or when Cdc42 was constitutively activated, phagocytic cup closure was impaired and endothelial cell invasion was inhibited. Thus, to complete invasion of the endothelium, staphylococci reorient recycling endocytic vesicles to recruit Cdc42GAP, which terminates Cdc42-induced actin polymerization in phagocytic cups. Analogous mechanisms might govern other Cdc42-dependent cell functions.

Indexed as

EndocytosisActinsBacterial Proteinscdc42 GTP-Binding ProteinEndosomesGene Knockdown TechniquesGTPase-Activating ProteinsHumansHuman Umbilical Vein Endothelial CellsPhagocytosisPolymerizationStaphylococcus aureusVesicular Transport ProteinsActinsARHGAP1 protein, humanBacterial Proteinscdc42 GTP-Binding ProteinGTPase-Activating ProteinsVesicular Transport ProteinsCdc42GAPEndotheliumPhagocytosisRecycling endosomesStaphylococci

Identifiers

PMID27311480
PMCPMC5004874
OpenAlexW2433641038

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.