Evidence map›Paper›PMID 21414240›Full record

ArticleGenetics research2011

Identifying a major locus that regulates spontaneous arthritis in IL-1ra-deficient mice and analysis of potential candidates.

Yan Jiao, Feng Jiao, Jian Yan, Qing Xiong, Daniel Shriner, Karen Hasty, John Stuart, Weikuan Gu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genetics research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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

8 authors at 3 institutions in 1 country.

Yan JiaoDepartment of Orthopaedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center (UTHSC), Memphis, TN 38163, USA.
Feng JiaoDepartment of Orthopaedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center (UTHSC), Memphis, TN 38163, USA.
Jian YanDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Qing XiongDepartment of Orthopaedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center (UTHSC), Memphis, TN 38163, USA.
Daniel ShrinerDepartment of Biostatistics, Section on Statistical Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Karen HastyDepartment of Orthopaedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center (UTHSC), Memphis, TN 38163, USA.
John StuartDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Weikuan GuDepartment of Orthopaedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center (UTHSC), Memphis, TN 38163, USA.
University of Tennessee Health Science Center · USCampbell Clinic · USUniversity of Alabama at Birmingham · US

Funding

MUTATION SCREENING OF SKELETAL DISEASE MOUSE MODELSR01AR051190 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI GU, WEIKUAN · 2004 to 2007
$1.1M
Pathogenic pathways involved in spontaneous arthritisR01AR050785 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI STUART, JOHN M · 2003 to 2006
$942k
NIAMS NIH HHS R01 AR050785NIAMS NIH HHS R01 AR051190NIAMS NIH HHS R01 AR50785NIAMS NIH HHS R01 AR51190
6 · The paper itself

Abstract

To identify genetic loci that regulate spontaneous arthritis in interleukin-1 receptor antagonist (IL-1ra)-deficient mice, an F2 population was created from a cross between Balb/c IL-1ra-deficient mice and DBA/1 IL-1ra-deficient mice. Spontaneous arthritis in the F2 population was examined and recorded. Genotypes of those F2 mice were determined using microsatellite markers. Quantitative trail locus (QTL) analysis was conducted with R/qtlbim. Functions of genes within QTL chromosomal regions were evaluated using a bioinformatics tool, PGMapper, and microarray analysis. Potential candidate genes were further evaluated using GeneNetwork. A total of 137 microsatellite markers with an average of 12 cM spacing along the whole genome were used for determining the correlation of arthritis phenotypes with genotypes of 191 F2 progenies. By whole-genome mapping, we obtained QTLs on chromosomes 1 and 6 that were above the significance threshold for strong Bayesian evidence. The QTL on chromosome 1 had a peak near D1Mit55 and D1Mit425 at 82·6 cM. It may account for as much as 12% of the phenotypic variation in susceptibility to spontaneous arthritis. The QTL region contained 208 known transcripts. According to their functions, Mr1, Pla2g4a and Fasl are outstanding candidate genes. From microarray analysis, 11 genes were selected as favourable candidates based on their function and expression profiles. Three of those 11 genes, Prg4, Ptgs2 and Mr1, correlated with the IL-1ra pathway. Those genes were considered to be the best candidates.

Indexed as

Genetic LinkageGenetic Predisposition to DiseaseQuantitative Trait LociAnimalsArthritisBiomarkersChromosome MappingComputational BiologyCrosses, GeneticCyclooxygenase 2DNAGene Expression ProfilingGenotypeHistocompatibility Antigens Class IIncidenceInterleukin 1 Receptor Antagonist ProteinBiomarkersCyclooxygenase 2DNAHistocompatibility Antigens Class IIl1rn protein, mouseInterleukin 1 Receptor Antagonist ProteinMinor Histocompatibility AntigensMr1 protein, mousePrg4 protein, mouseProteoglycan 4ProteoglycansPtgs2 protein, mouse

Identifiers

PMID21414240
PMCPMC3245888
OpenAlexW2045878195

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.