Evidence map›Paper›PMID 24847357›Full record

ArticleFrontiers in genetics2014

Genome wide association study of SNP-, gene-, and pathway-based approaches to identify genes influencing susceptibility to Staphylococcus aureus infections.

Zhan Ye, Daniel A Vasco, Tonia C Carter, Murray H Brilliant, Steven J Schrodi, Sanjay K Shukla

Abstract read
In one paragraph

Article in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Susceptibility to Childhood Pneumonia: A Genome-Wide Analysis.American journal of respiratory cell and molecular biology · 2017
    Trial
  2. iScience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Frontiers in microbiomes · 2024
    Article
  8. Article
  9. Persistent Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. The adverse impact of cadmium on immune function and lung host defense.Seminars in cell & developmental biology · 2021
    Article
  14. Review
  15. Genomic analyses ofMicrobial genomics · 2020
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Fulminant Staphylococcal Infections.Microbiology spectrum · 2018
    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

6 authors.

Zhan YeBiomedical Informatics Research Center, Marshfield Clinic Research Foundation Marshfield, WI, USA.
Daniel A VascoCenter for Human Genetics, Marshfield Clinic Research Foundation Marshfield, WI, USA.
Tonia C CarterCenter for Human Genetics, Marshfield Clinic Research Foundation Marshfield, WI, USA.
Murray H BrilliantCenter for Human Genetics, Marshfield Clinic Research Foundation Marshfield, WI, USA.
Steven J SchrodiCenter for Human Genetics, Marshfield Clinic Research Foundation Marshfield, WI, USA.
Sanjay K ShuklaCenter for Human Genetics, Marshfield Clinic Research Foundation Marshfield, WI, USA.

Funding

Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
JH/CIDR Genotyping for Genome-Wide Association StudiesU01HG004438 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID · 2007 to 2011
$24.2M
Genome-Wide Study of Cataract and Low HDL in the Personalized Medicine Research PU01HG004608 · NHGRI · MARSHFIELD CLINIC RESEARCH FOUNDATION · PI MCCARTY, CATHERINE ANNE · 2007 to 2010
$3.3M
NCATS NIH HHS UL1 TR000427NCRR NIH HHS UL1 RR025011NHGRI NIH HHS U01 HG004438NHGRI NIH HHS U01 HG004608
6 · The paper itself

Abstract

backgroundWe conducted a genome-wide association study (GWAS) to identify specific genetic variants that underlie susceptibility to diseases caused by Staphylococcus aureus in humans.

methodsCases (n = 309) and controls (n = 2925) were genotyped at 508,921 single nucleotide polymorphisms (SNPs). Cases had at least one laboratory and clinician confirmed disease caused by S. aureus whereas controls did not. R-package (for SNP association), EIGENSOFT (to estimate and adjust for population stratification) and gene- (VEGAS) and pathway-based (DAVID, PANTHER, and Ingenuity Pathway Analysis) analyses were performed.

resultsNo SNP reached genome-wide significance. Four SNPs exceeded the p < 10(-5) threshold including two (rs2455012 and rs7152530) reaching a p-value < 10(-7). The nearby genes were PDE4B (rs2455012), TXNRD2 (rs3804047), VRK1 and BCL11B (rs7152530), and PNPLA5 (rs470093). The top two findings from the gene-based analysis were NMRK2 (p gene = 1.20E-05), which codes an integrin binding molecule (focal adhesion), and DAPK3 (p gene = 5.10E-05), a serine/threonine kinase (apoptosis and cytokinesis). The pathway analyses identified epithelial cell responses to mechanical and non-mechanical stress.

conclusionWe identified potential susceptibility genes for S. aureus diseases in this preliminary study but confirmation by other studies is needed. The observed associations could be relevant given the complexity of S. aureus as a pathogen and its ability to exploit multiple biological pathways to cause infections in humans.

Indexed as

disease susceptibilityGWASintegrin and keratin disease pathwayskin and soft tissue infectionStaphylococcus aureus

Identifiers

PMID24847357
PMCPMC4023021

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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.