Evidence map›Paper›PMID 27572444›Full record

ArticleNature microbiology2016

Intermediate filaments enable pathogen docking to trigger type 3 effector translocation.

Brian C Russo, Luisa M Stamm, Matthijs Raaben, Caleb M Kim, Emily Kahoud, Lindsey R Robinson, Sayantan Bose, Ana L Queiroz, Bobby Brooke Herrera, Leigh A Baxt and 6 more

Open access · greenAbstract read
In one paragraph

Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 60 citations in OpenAlex.

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  17. The T3SS ofMicroorganisms · 2020
    Review
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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

16 authors at 3 institutions in 1 country.

Brian C RussoDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Luisa M StammDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Matthijs RaabenDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Caleb M KimDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Emily KahoudDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Lindsey R RobinsonDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Sayantan BoseDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.ORCID http://orcid.org/0000-0003-2397-4740
Ana L QueirozDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Bobby Brooke HerreraDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Leigh A BaxtDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Nirit Mor-VakninDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
Yang FuDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Gabriel MolinaDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
David M MarkovitzDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.
Sean P WhelanDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Marcia B GoldbergDivision of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Harvard University · USMassachusetts General Hospital · USUniversity of Michigan · US

Funding

Treatments for Nipah Virus InfectionU54AI057159 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WHELAN, SEAN PJ · 2003 to 2013
$113.7M
Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ANDREW D LUSTER · 1991 to 2026
$35.3M
INFECTIOUS DISEASE AND BASIC MICROBIOLOGICAL MECHANISMST32AI007061 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 1985 to 2026
$12.1M
Molecular signaling in Shigella disseminationR01AI081724 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 2010 to 2026
$7.1M
Molecular Mechanisms of Modulation of N-WASP activityF32AI092967 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI BAXT, LEIGH A. · 2011 to 2013
$142k
Role of host factors during effector translocation by type III secretionF32AI114162 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RUSSO, BRIAN · 2016 to 2017
$84k
NIAID NIH HHS F32 AI092967NIAID NIH HHS F32 AI114162NIAID NIH HHS L40 AI113818NIAID NIH HHS R01 AI081724NIAID NIH HHS T32 AI007061NIAID NIH HHS U54 AI057159NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Type 3 secretion systems (T3SSs) of bacterial pathogens translocate bacterial effector proteins that mediate disease into the eukaryotic cytosol. Effectors traverse the plasma membrane through a translocon pore formed by T3SS proteins. In a genome-wide selection, we identified the intermediate filament vimentin as required for infection by the T3SS-dependent pathogen S. flexneri. We found that vimentin is required for efficient T3SS translocation of effectors by S. flexneri and other pathogens that use T3SS, Salmonella enterica serovar Typhimurium and Yersinia pseudotuberculosis. Vimentin and the intestinal epithelial intermediate filament keratin 18 interact with the C-terminus of the Shigella translocon pore protein IpaC. Vimentin and its interaction with IpaC are dispensable for pore formation, but are required for stable docking of S. flexneri to cells; moreover, stable docking triggers effector secretion. These findings establish that stable docking of the bacterium specifically requires intermediate filaments, is a process distinct from pore formation, and is a prerequisite for effector secretion.

Indexed as

Bacterial AdhesionAnimalsAntigens, BacterialCell LineHost-Pathogen InteractionsHumansKeratin-18MiceProtein BindingProtein TransportSalmonella typhimuriumShigella flexneriType III Secretion SystemsVimentinVirulence FactorsYersinia pseudotuberculosisAntigens, BacterialIpaC protein, ShigellaKeratin-18Type III Secretion SystemsVimentinVirulence Factors

Identifiers

PMID27572444
PMCPMC5006386
OpenAlexW2325722152

What OpenQuestion holds

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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.