ArticleHuman molecular genetics2015
Gpr126/Adgrg6 deletion in cartilage models idiopathic scoliosis and pectus excavatum in mice.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Genome-wide meta-analysis and replication studies in multiple ethnicities identify novel adolescent idiopathic scoliosis susceptibility loci.Human molecular genetics · 2018Pooled it
- Massively parallel characterization of adolescent idiopathic scoliosis risk variants.Genome research · 2026Article
- Non-coding regulatory variants in adolescent idiopathic scoliosis risk and pathogenesis.Communications biology · 2026Review
- Integrated transcriptomic and functional analysis reveals tissue-specific molecular pathology in adolescent idiopathic scoliosis.HGG advances · 2026Article
- The therapeutic potential of orphan adhesion G-protein-coupled receptors.Nature reviews. Drug discovery · 2026Review
- FLNB and TTC26 regulate ciliary Hedgehog signaling to maintain intervertebral disc matrix homeostasis in adolescent idiopathic scoliosis.Genome biology · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Genetic interaction betweenResearch square · 2026Article
- Genetic interaction betweenbioRxiv : the preprint server for biology · 2026Article
- Adgrg6/Gpr126 is required for compact wall integrity and establishing trabecular identity during cardiac trabeculation.Nature communications · 2026Article
- Extra-helical allosteric binding site of apomorphine in ADGRG6.Cell discovery · 2026Article
- Genetic Associations with Pectus Excavatum: A Systematic Review.Current issues in molecular biology · 2026Review
- Expanding and refining the Mammalian Phenotype Ontology to enhance disease model discovery.Disease models & mechanisms · 2025Article
- Oxidative stress-induced intervertebral disc remodelling and elevated stiffness drive idiopathic scoliosis in preclinical models.Nature communications · 2025Article
- The importance of imperfect pre-clinical models in adolescent idiopathic scoliosis.Disease models & mechanisms · 2025Review
- Mechanosensitive adhesion G protein-coupled receptors: Insights from health and disease.Genes & diseases · 2025Review
- Variants in the SOX9 transactivation middle domain induce axial skeleton dysplasia and scoliosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The G protein-coupled receptor ADGRG6 maintains mouse growth plate homeostasis through IHH signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Article
- Adhesion G Protein-Coupled ReceptorCells · 2024Article
7 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Adolescent idiopathic scoliosis (AIS) and pectus excavatum (PE) are common pediatric musculoskeletal disorders. Little is known about the tissue of origin for either condition, or about their genetic bases. Common variants near GPR126/ADGRG6 (encoding the adhesion G protein-coupled receptor 126/adhesion G protein-coupled receptor G6, hereafter referred to as GPR126) were recently shown to be associated with AIS in humans. Here, we provide genetic evidence that loss of Gpr126 in osteochondroprogenitor cells alters cartilage biology and spinal column development. Microtomographic and x-ray studies revealed several hallmarks of AIS, including postnatal onset of scoliosis without malformations of vertebral units. The mutants also displayed a dorsal-ward deflection of the sternum akin to human PE. At the cellular level, these defects were accompanied by failure of midline fusion within the developing annulus fibrosis of the intervertebral discs and increased apoptosis of chondrocytes in the ribs and vertebrae. Molecularly, we found that loss of Gpr126 upregulated the expression of Gal3st4, a gene implicated in human PE, encoding Galactose-3-O-sulfotransferase 4. Together, these data uncover Gpr126 as a genetic cause for the pathogenesis of AIS and PE in a mouse model.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.