Evidence map›Paper›PMID 26867180›Full record

ArticleCell host & microbe2016

A Bacterial Pathogen Targets a Host Rab-Family GTPase Defense Pathway with a GAP.

Stefania Spanò, Xiang Gao, Sebastian Hannemann, María Lara-Tejero, Jorge E Galán

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 130 citations in OpenAlex.

  1. The Manipulation of Host Cells byInternational journal of molecular sciences · 2026
    Review
  2. Host prenylation promotes membrane association of theMicrobiology (Reading, England) · 2026
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  4. Molecular strategies ofFrontiers in cellular and infection microbiology · 2026
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  12. Review
  13. The interplay betweenCell insight · 2025
    Review
  14. International journal of molecular sciences · 2025
    Review
  15. Article
  16. mSphere · 2024
    Article
  17. Review
  18. Article
  19. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Functional Divergence of the ParalogInternational journal of molecular sciences · 2024
    Review

29 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Stefania SpanòDepartment of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA. Electronic address: stefania.spano@abdn.ac.uk.
Xiang GaoDepartment of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
Sebastian HannemannDepartment of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
María Lara-TejeroDepartment of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
Jorge E GalánDepartment of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA. Electronic address: jorge.galan@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Host Cell Signaling Pathways Induced By SalmonellaR01AI055472 · NIAID · YALE UNIVERSITY · PI Jorge E Galan · 2003 to 2026
$13.2M
Typhoid Toxin and Salmonella Typhi pathogenesisR01AI114618 · NIAID · YALE UNIVERSITY · PI GALAN, JORGE E · 2014 to 2023
$5.4M
Virulence factors of Salmonella TyphiR01AI079022 · NIAID · YALE UNIVERSITY · PI GALAN, JORGE E · 2008 to 2012
$2.0M
Virulence factors of Salmonella TyphiR56AI079022 · NIAID · YALE UNIVERSITY · PI GALAN, JORGE E · 2014 to 2014
$486k
NCATS NIH HHS UL1 TR001863NIAID NIH HHS AI055472NIAID NIH HHS AI079022NIAID NIH HHS R01 AI055472NIAID NIH HHS R01 AI079022NIAID NIH HHS R01 AI114618NIAID NIH HHS R56 AI079022
6 · The paper itself

Abstract

Cell-autonomous defense mechanisms are potent strategies that protect individual cells against intracellular pathogens. The Rab-family GTPase Rab32 was previously shown to restrict the intracellular human pathogen Salmonella Typhi, but its potential broader role in antimicrobial defense remains unknown. We show that Rab32 represents a general cell-autonomous, antimicrobial defense that is counteracted by two Salmonella effectors. Mice lacking Rab-32 or its nucleotide exchange factor BLOC-3 are permissive to S. Typhi infection and exhibit increased susceptibility to S. Typhimurium. S. Typhimurium counters this defense pathway by delivering two type III secretion effectors, SopD2, a Rab32 GAP, and GtgE, a specific Rab32 protease. An S. Typhimurium mutant strain lacking these two effectors exhibits markedly reduced virulence, which is fully restored in BLOC-3-deficient mice. These results demonstrate that a cell-autonomous, Rab32-dependent host defense pathway plays a central role in the defense against vacuolar pathogens and describe a mechanism evolved by a bacterial pathogen to counter it.

Indexed as

AnimalsBacterial ProteinsHost-Pathogen InteractionsHumansMiceProteolysisrab GTP-Binding ProteinsSalmonella InfectionsSalmonella typhiSalmonella typhimuriumVirulenceBacterial ProteinsRab32 protein, mouserab GTP-Binding Proteinsbacterial pathogenesiscell-autonomous defenseinnate immunitylysosome-related organelleslysosomesmacrophagesmembrane trafficRab32Rab GTPasesSalmonella pathogenesisSalmonella Typhitype III secretiontyphoid fever

Identifiers

PMID26867180
PMCPMC4854434
OpenAlexW2266433488

What OpenQuestion holds

Textmetadata
LicenceTDM
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.