Ask about this productRelated genes to: Slc26a2 Blocking Peptide
- Gene:
- SLC26A2 NIH gene
- Name:
- solute carrier family 26 member 2
- Previous symbol:
- DTD
- Synonyms:
- DTDST
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: Slc26a2 Blocking Peptide
Related articles to: Slc26a2 Blocking Peptide
- Osteoarthritis (OA) is a common degenerative joint disease with no curative treatments and a poorly understood etiology. Here, we report that defective sulfation, a largely underexplored chemical modification of lipid metabolites, drives pathogenic lipid accumulation in chondrocytes to promote OA. Intrigued by observations of lipid droplet accumulation in cartilage from genetically modified male mice with sulfation defects, we identified that the production and sulfation status of 25-hydroxycholesterol (25HC), an oxysterol metabolite, could impact OA risk and development. Transcriptomics and peptide-centric local stability assays revealed that 25HC and its sulfated derivative (25HC3S) exhibited opposing regulatory effects on lipid biosynthesis genes and distinct protein interaction profiles. Mechanistically, 25HC activated Liver X Receptor (LXR) ligand-dependently to potentiate lipid synthesis and uptake, while 25HC3S deactivated LXR by altering its nuclear localization and promoting nucleolar sequestration, thus mitigating chondrocyte lipid accumulation and cartilage damage. Moreover, human studies linked genetic variants in 25HC sulfation pathways to OA risk, with concomitantly reduced sulfation gene expression and increased lipid accumulation in OA cartilage. These findings support an oxysterol undersulfation model wherein defective oxysterol sulfation unleashes nuclear oxysterol receptor activation to drive pathogenic chondrocyte lipid accumulation, and highlight the therapeutic potential of 25HC3S against OA. - Source: PubMed
Publication date: 2026/05/19
Wang HuanboNi BoweiQian YuDing GuangyuHe TingZhang XinyuXu HailunHao XueHu YaqianWang DiJie QiangLi YingJie TianyangLi Zhong AlanLuo ZhuojingZheng HoufengYang LiuZheng Chao - Tungsten is an emerging environmental contaminant, highlighting the urgent need to elucidate its toxicological characteristics and assess long-term health risks. Our previous investigations show that tungsten deposition in the bone is associated with stalled pre-B lymphocyte differentiation, inhibition of osteogenesis, and increased intervertebral disc degeneration and fibrosis. To delineate the underlying molecular mechanisms, we employed CRISPR-based genomics on NALM-6 cells and identified Solute Carrier Family 26 Member 2 (SLC26A2), a sulfate/chloride antiporter, as a pivotal mediator of tungsten-induced toxicity. SLC26A2 deletion reduced tungsten-induced growth inhibition and intercellular tungsten levels. Functional impairment of SLC26A2 is associated with chondrodysplasias, thus, we hypothesized that tungsten would impair the development of cartilage and bone tissues. Indeed, tungstate exposure impaired chondrogenesis and osteogenesis in murine limb cultures, which was reversible by sulfate supplementation. Our study demonstrates that tungsten exploits SLC26A2 for cellular entry and correlates with bone development disruption through proteoglycan and collagen depletion. - Source: PubMed
Publication date: 2026/05/12
Bakadlag RowaLi SheenaGuilbert CynthiaHuard CarolineBertomeu ThierryCoulombe-Huntington JasminJackson Brian PGrant Michael PIskandarani LamaPaganini ChiaraRossi AntonioMwale FacksonTyers MikeHales Barbara FMann Koren K - Hepatocellular carcinoma (HCC) faces a critical shortage of prognostic biomarkers and therapeutic targets. While solute carrier family 26 member 2 (SLC26A2) is known to be involved in skeletal disorders and even tumors, its specific role in HCC pathogenesis remains undefined. - Source: PubMed
Publication date: 2026/05/08
Wang RuiZhang XijieRen BoZhou Wence - Proteoglycans are a major component of the connective tissue matrix, which consists of a core protein and covalently attached glycosaminoglycan (GAG) chains, which are highly sulfated polysaccharides with a tetrasaccharide linker for the core protein attachment. Impaired synthesis or degradation of GAG causes genetic disorders. In the 1950s, deficient lysosomal GAG degradation was discovered in mucopolysaccharidoses. In the 1990s, a defective enzyme for GAG synthesis was implicated in a variant of Ehlers-Danlos syndrome and an impaired GAG sulfation in diastrophic dysplasia. Newer studies have uncovered that abnormal GAG synthesis causes a large group of genetic skeletal disorders with joint and skin abnormalities. - Source: PubMed
Publication date: 2026/02/26
Tsujioka YukoSimsek Kiper Pelin OzlemUnger SheilaHanda AtsuhikoKono TatsuoJinzaki MasahiroRossi AntonioSuperti-Furga AndreaNishimura Gen - Multiple epiphyseal dysplasia (MED) is a clinically and genetically heterogeneous group of disorders characterized by a waddling gait, joint pain, and early-onset osteoarthritis. The aim of this study was to compare the genetic characteristics and long-term clinical follow-up findings of 22 patients with MED from 17 unrelated families. Molecular diagnosis was performed using clinical exome analysis and exome sequencing. Seventeen children were followed for a median of 5.5 years. Eighteen disease-related variants were identified: 47% in , 11.8% each in and in a monoallelic state, 17.6% in , and 11.8% each in and in a biallelic state. Some mutations previously identified in pseudoachondroplasia, an allelic disorder of MED1, were shown in our study to exhibit a typical MED1 or intermediate phenotype. In contrast, it was confirmed that certain mutations in lead to MED4 phenotype. Furthermore, it has been observed that biallelic variants in may be associated with the MED5 phenotype. In patients with MED2 and MED3, the knee joint is affected, while in other types, the hip joint is predominantly affected. In 15 children followed until ages 11-18, height decreased slightly as they grew older but remained normal or at the lower limit, and slow progression was observed in the waddling gait and joint pain, except in the intermediate form. This study reveals the frequency of disease-related variants, including seven novel ones, in genes leading to MED1-5 and 7 phenotypes, and expands the spectrum of genetic and clinical phenotypes. - Source: PubMed
Publication date: 2026/04/15
Taner Hasan EmirUludağ Alkaya DilekKalyoncu Uçar AyşeŞeker AliCentel TuncayYıldırım TimurGüneş NilayTüysüz Beyhan