ArticleNature communications2019
Genome-scale Capture C promoter interactions implicate effector genes at GWAS loci for bone mineral density.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
97 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Bone mineral density loci specific to the skull portray potential pleiotropic effects on craniosynostosis.Communications biology · 2023Pooled it
- Multi-ancestry genetic study of type 2 diabetes highlights the power of diverse populations for discovery and translation.Nature genetics · 2022Pooled it
- Integrative genomics and single-cell CRISPRi screening dissect Alzheimer GWAS non-coding variants regulating TSPAN14.American journal of human genetics · 2026Article
- Regional heterogeneity in phenotypic and genetic associations between bone and brain in humans.Nature communications · 2026Article
- Cell-specific variant-to-gene mapping identifies conserved neural and glial regulators of sleep.bioRxiv : the preprint server for biology · 2026Article
- Variant-to-gene mapping identifiesbioRxiv : the preprint server for biology · 2026Article
- Chaperone-mediated autophagy sustains pericyte stemness necessary for brain tissue homeostasis.Journal of advanced research · 2026Article
- Osteoporosis After Menopause and After Drug Therapy: The Molecular Mechanism of Bone Loss and Its Treatment.International journal of molecular sciences · 2026Review
- 3D chromatin-based variant-to-gene maps across 57 human cell types reveal the cellular and genetic architecture of autoimmune disease susceptibility.Genome biology · 2025Article
- Review
- Large-scale multiomic analysis identifies non-coding somatic driver mutations and nominatesGut · 2025Article
- GWAS-informed data integration and non-coding CRISPRi screen illuminate genetic etiology of bone mineral density.Genome biology · 2025Article
- Recent Advances in Experimental Functional Characterization of GWAS Candidate Genes in Osteoporosis.International journal of molecular sciences · 2025Review
- Mapping chromatin interactions at melanoma susceptibility loci uncovers distant cis-regulatory gene targets.American journal of human genetics · 2025Article
- Genetic effects on chromatin accessibility uncover mechanisms of liver gene regulation and quantitative traits.Genome research · 2025Article
- Mapping HIV-1 RNA structure, homodimers, long-range interactions and persistent domains by HiCapR.eLife · 2025Article
- Shared and unique 3D genomic features of substance use disorders across multiple cell types.medRxiv : the preprint server for health sciences · 2025Article
- Regulation of WNT16 in bone may involve upstream enhancers within CPED1.Scientific reports · 2025Article
- Loss ofJBMR plus · 2025Article
- Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Osteoporosis is a devastating disease with an essential genetic component. GWAS have discovered genetic signals robustly associated with bone mineral density (BMD), but not the precise localization of effector genes. Here, we carry out physical and direct variant to gene mapping in human mesenchymal progenitor cell-derived osteoblasts employing a massively parallel, high resolution Capture C based method in order to simultaneously characterize the genome-wide interactions of all human promoters. By intersecting our Capture C and ATAC-seq data, we observe consistent contacts between candidate causal variants and putative target gene promoters in open chromatin for ~ 17% of the 273 BMD loci investigated. Knockdown of two novel implicated genes, ING3 at 'CPED1-WNT16' and EPDR1 at 'STARD3NL', inhibits osteoblastogenesis, while promoting adipogenesis. This approach therefore aids target discovery in osteoporosis, here on the example of two relevant genes involved in the fate determination of mesenchymal progenitors, and can be applied to other common genetic diseases.
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Registered trials
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