ArticleEBioMedicine2019
Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Multi-Breed Genome-Wide Association Analysis Reveals Candidate Genes for Growth and Body Conformation Traits in Four Populations of Native and Crossbred Chinese Sheep.Animals : an open access journal from MDPI · 2026Article
- Oxysterol undersulfation promotes osteoarthritis by fueling chondrocyte lipid accumulation.Nature communications · 2026Article
- SLC26A2 as a key regulator and therapeutic target in hepatocellular carcinoma: evidence from pan-cancer and mechanistic studies.Human genomics · 2026Article
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Clinical and molecular characterization of chondrodysplasias in a cohort of Egyptian patients.Scientific reports · 2025Article
- Melatonin amelioratesGenes & diseases · 2025Article
- Article
- Slc26a2-mediated sulfate metabolism is important in tooth development.Disease models & mechanisms · 2024Article
- Protein phosphatase SCP4 regulates cartilage development and endochondral osteogenesis via FoxO3a dephosphorylation.Cell proliferation · 2024Article
- Biallelic variants in SLC26A2 cause multiple epiphyseal dysplasia-4 by disturbing chondrocyte homeostasis.Orphanet journal of rare diseases · 2024Article
- Molecular landscape of congenital vertebral malformations: recent discoveries and future directions.Orphanet journal of rare diseases · 2024Review
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Targeting FGFR3 signaling and drug repurposing for the treatment of SLC26A2-related chondrodysplasia in mouse model.Journal of orthopaedic translation · 2024Article
- Article
- Article
- Article
- SLC26 family: a new insight for kidney stone disease.Frontiers in physiology · 2023Review
- Analyze Mouse Knockout Models of UPR Pathway Elements.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Genomic adaptation of Ethiopian indigenous cattle to high altitude.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in the SLC26A2 gene cause a spectrum of currently incurable human chondrodysplasias. However, genotype-phenotype relationships of SLC26A2-deficient chondrodysplasias are still perplexing and thus stunt therapeutic development.
methodsTo investigate the causative role of SLC26A2 deficiency in chondrodysplasias and confirm its skeleton-specific pathology, we generated and analyzed slc26a2
findingsTwo lethal forms of human SLC26A2-related chondrodysplasias, achondrogenesis type IB (ACG1B) and atelosteogenesis type II (AO2), are phenocopied by slc26a2
interpretationOur study unveils a previously unrecognized pathogenic mechanism underlying ACG1B and AO2, and supports suppression of FGFR3 signaling as a promising therapeutic approach for SLC26A2-related chondrodysplasias. FUND: This work was supported by National Natural Science Foundation of China (81871743, 81730065 and 81772377).
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