Evidence map›Paper›PMID 32041354›Full record

ArticleToxins2020

Host-Receptor Post-Translational Modifications Refine Staphylococcal Leukocidin Cytotoxicity.

Angelino T Tromp, Michiel Van Gent, Joris P Jansen, Lisette M Scheepmaker, Anneroos Velthuizen, Carla J C De Haas, Kok P M Van Kessel, Bart W Bardoel, Michael Boettcher, Michael T McManus and 4 more

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.2field-weighted citation impact, top 34% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Toxins · 2021
    Article
  12. Toxins · 2020
    Review
  13. Review
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

14 authors at 2 institutions in 3 countries.

Angelino T TrompDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Michiel Van GentDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Joris P JansenDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Lisette M ScheepmakerDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Anneroos VelthuizenDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Carla J C De HaasDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Kok P M Van KesselDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Bart W BardoelDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Michael BoettcherDepartment of Microbiology and Immunology, UCSF Diabetes Center, Keck Center for Noncoding RNA, University of California, San Francisco, San Francisco, CA 94143, USA.
Michael T McManusDepartment of Microbiology and Immunology, UCSF Diabetes Center, Keck Center for Noncoding RNA, University of California, San Francisco, San Francisco, CA 94143, USA.
Jos A G Van StrijpDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Robert Jan LebbinkDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
Pieter-Jan A HaasDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
András N SpaanDepartment of Medical Microbiology, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands.
University Medical Center Utrecht · NLUniversity of California, San Francisco · US

Funding

KWF Kankerbestrijding UU 2012-5667
6 · The paper itself

Abstract

Staphylococcal bi-component pore-forming toxins, also known as leukocidins, target and lyse human phagocytes in a receptor-dependent manner. S-components of the leukocidins Panton-Valentine leukocidin (PVL), γ-haemolysin AB (HlgAB) and CB (HlgCB), and leukocidin ED (LukED) specifically employ receptors that belong to the class of G-protein coupled receptors (GPCRs). Although these receptors share a common structural architecture, little is known about the conserved characteristics of the interaction between leukocidins and GPCRs. In this study, we investigated host cellular pathways contributing to susceptibility towards

Indexed as

Protein Processing, Post-TranslationalCell Culture TechniquesCell SurvivalCRISPR-Cas SystemsDrug Resistance, BacterialGenetic Predisposition to DiseaseGenome-Wide Association StudyHEK293 CellsHost Microbial InteractionsHumansLeukocidinsPhagocytesProtein BindingReceptors, G-Protein-CoupledStaphylococcal InfectionsStaphylococcus aureusLeukocidinsReceptors, G-Protein-Coupledbi-component pore-forming toxinsG-protein coupled receptorsleukocidinspost-translational modificationsreceptorsStaphylococcus aureus

Identifiers

PMID32041354
PMCPMC7076806
OpenAlexW3004690201

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.