ArticleNature genetics2012
Bayesian inference analyses of the polygenic architecture of rheumatoid arthritis.
Article in Nature genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 11 of them syntheses that pooled it.
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Who cites it
236 citing papers in PubMed, 11 syntheses or guidelines pooled it.
- Incorporating functional priors improves polygenic prediction accuracy in UK Biobank and 23andMe data sets.Nature communications · 2021Pooled it
- Prioritization of causal genes for coronary artery disease based on cumulative evidence from experimental and in silico studies.Scientific reports · 2020Pooled it
- Validation of Polygenic Scores for QT Interval in Clinical Populations.Circulation. Cardiovascular genetics · 2017Pooled it
- Transethnic meta-analysis identifiesAnnals of the rheumatic diseases · 2017Pooled it
- Genome-wide association studies in the Japanese population identify seven novel loci for type 2 diabetes.Nature communications · 2016Pooled it
- Functional implications of disease-specific variants in loci jointly associated with coeliac disease and rheumatoid arthritis.Human molecular genetics · 2016Pooled it
- Systems Genetics Analysis of Genome-Wide Association Study Reveals Novel Associations Between Key Biological Processes and Coronary Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Pooled it
- Genome-wide trans-ancestry meta-analysis provides insight into the genetic architecture of type 2 diabetes susceptibility.Nature genetics · 2014Pooled it
- The influence of polygenic risk scores on heritability of anti-CCP level in RA.Genes and immunity · 2014Pooled it
- Pooled it
- Predicting risk of type 2 diabetes mellitus with genetic risk models on the basis of established genome-wide association markers: a systematic review.American journal of epidemiology · 2013Pooled it
- Association of polymorphisms in interleukin (IL)-12A and -B genes with rheumatoid arthritis in a Chinese population.Clinical and experimental immunology · 2015Trial
- Principled measures and estimates of trait polygenicity.American journal of human genetics · 2026Article
- Early and late RNA eQTL are driven by different genetic mechanisms.Nature communications · 2026Article
- Representation in genetic studies affects inference about genetic architecture.bioRxiv : the preprint server for biology · 2026Article
- Rheumatoid Arthritis: A Comprehensive Review of Etiology, Pathophysiology, and Innovative Therapeutic Advancements.Current pharmaceutical design · 2026Review
- Incorporating multiple functional annotations to improve polygenic risk prediction accuracy.Cell genomics · 2025Article
- A scalable variational inference approach for increased mixed-model association power.Nature genetics · 2025Article
- Identification of epistatic SNP combinations in rheumatoid arthritis using LAMPLINK and Japanese cohorts.Journal of human genetics · 2024Article
- BLUPmrMLM: A Fast mrMLM Algorithm in Genome-wide Association Studies.Genomics, proteomics & bioinformatics · 2024Article
176 more citing papers are in PubMed but not listed here.
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21 authors.
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Abstract
The genetic architectures of common, complex diseases are largely uncharacterized. We modeled the genetic architecture underlying genome-wide association study (GWAS) data for rheumatoid arthritis and developed a new method using polygenic risk-score analyses to infer the total liability-scale variance explained by associated GWAS SNPs. Using this method, we estimated that, together, thousands of SNPs from rheumatoid arthritis GWAS explain an additional 20% of disease risk (excluding known associated loci). We further tested this method on datasets for three additional diseases and obtained comparable estimates for celiac disease (43% excluding the major histocompatibility complex), myocardial infarction and coronary artery disease (48%) and type 2 diabetes (49%). Our results are consistent with simulated genetic models in which hundreds of associated loci harbor common causal variants and a smaller number of loci harbor multiple rare causal variants. These analyses suggest that GWAS will continue to be highly productive for the discovery of additional susceptibility loci for common diseases.
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