Ask about this productRelated genes to: SLCO2A1 antibody
- Gene:
- SLCO2A1 NIH gene
- Name:
- solute carrier organic anion transporter family member 2A1
- Previous symbol:
- SLC21A2, MATR1
- Synonyms:
- PGT, OATP2A1
- Chromosome:
- 3q22.1-q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2019-04-23
Related products to: SLCO2A1 antibody
Related articles to: SLCO2A1 antibody
- Primary hypertrophic osteoarthropathy (PHO), also known as pachydermoperiostosis, is a rare genetic disorder with autosomal inheritance. We present the case of a 31-year-old male with a disease onset at 12 years of age, initially presenting as digital clubbing of the hands and feet and ankle joint hypertrophy. The clinical phenotype progressed significantly by age 17, with the development of marked facial skin thickening, deepened centripetal skin folds, a corrugated scalp, hypertrophic alae nasi, acne, ptosis, and palmoplantar hyperhidrosis. Anemia was identified at age 19, accompanied by persistent fatigue, followed by the onset of bilateral knee joint pain two years later. Fluorine-18-fluorodeoxyglucose (F-FDG) positron emission tomography/computed tomography (PET/CT) imaging revealed a constellation of findings that can be grouped into three categories: (1) skeletal: cortical thickening and periosteal reaction in the long bones of the lower limbs, along with extensively increased bone marrow density throughout the skeleton; (2) soft tissue: diffuse thickening of the cranial and facial skin, and multiple para-spinal soft tissue foci; and (3) systemic: cardiac findings suggestive of anemia-related adaptation. Genetic analysis confirmed the diagnosis by identifying heterozygous mutations in the SLCO2A1 gene (c.290G>A [p.R97H] and c.1295+1G>A), establishing PHO complicated by anemia. - Source: PubMed
Publication date: 2026/08/06
Wang DaoyingWang ZhimingLi Haiyang - : Chronic enteropathy associated with the gene (CEAS) is a rare disease characterized by multiple small intestinal ulcers whose pathogenesis remains poorly understood. This study aimed to characterize the proteomic and phosphoproteomic profiles of CEAS and to identify molecular pathways involved in its pathogenesis. : Quantitative proteomics and phosphoproteomics were performed on intestinal mucosal tissues from patients with CEAS ( = 3), Crohn's disease (CD, = 3), and healthy controls ( = 3). Differentially expressed proteins (DEPs) and differentially phosphorylated proteins (DPPs) were analyzed using functional enrichment, gene set enrichment analysis (GSEA), protein-protein interaction (PPI) networks, and integrative analysis. : A total of 900 DEPs were identified in CEAS and 277 in CD relative to controls, including 717 CEAS-specific proteins. CEAS-specific alterations were strongly enriched in focal adhesion and extracellular matrix-related pathways, whereas shared proteins between CEAS and CD were primarily associated with epithelial barrier function, including tight junction and adherens junction pathways. GSEA revealed that CEAS was characterized by upregulation of tissue remodeling and focal adhesion pathways, accompanied by suppression of digestive and metabolic processes, while CD exhibited prominent adaptive immune activation. PPI network analysis identified , , , and as candidate hub proteins; however, none retained significance after FDR correction, whereas brush-border components (, , , ) and actin cytoskeletal regulators remained the most statistically robust alterations. Integrated analysis further highlighted focal adhesion-related proteins with coordinated expression and phosphorylation changes. : This exploratory study provides the first integrative proteomic and phosphoproteomic characterization of CEAS, suggesting that impairment of the intestinal brush border and mucosal barrier, together with actin cytoskeletal reorganization, may distinguish CEAS from immune-dominant CD. These findings are hypothesis-generating and require validation in larger cohorts. - Source: PubMed
Publication date: 2026/06/23
Xie ZhixinHan TaotaoWu DongLi JingnanYang AimingLi YueWang Qiang - Prostaglandin E2 (PGE2) plays diverse roles in secondary injury after ischemic stroke. Solute carrier organic anion transporter family member 2A1 (SLCO2A1) is a key transporter of PGE2; however, its role in the pathophysiology of cerebral ischemia remains largely unknown. Here, we report that ischemia induces transient upregulation of SLCO2A1 in reactive astrocytes. Local knockdown of Slco2a1 in astrocytes disrupted astrocyte-endothelial cell contact, resulting in extravascular IgG accumulation and exacerbated functional deficits. In contrast, overexpression of SLCO2A1 in astrocytes significantly reduced blood-brain barrier (BBB) disruption and promoted locomotor recovery. Mechanistically, intracellular Ca signaling, rather than E2 prostanoid receptor signaling, was further amplified in Slco2a1-knockdown astrocytes and suppressed in SLCO2A1-overexpressing astrocytes following oxygen-glucose deprivation. Both pharmacological and chemogenetic manipulation of intracellular or astrocytic Ca effectively counteracted the effects of SLCO2A1 activity on BBB permeability and functional recovery. These data reveal a protective role of astrocytic SLCO2A1-Ca signaling in maintaining BBB integrity after ischemic stroke. - Source: PubMed
Publication date: 2026/07/27
Wang TaozhiYang ManpingGuo HaiyunMa HongyuLi ZhenzhenKang JunjunGuo YaominWu ShengxiWang YazhouHou Wugang - Primary hypertrophic osteoarthropathy (PHO) is a rare hereditary clinical syndrome characterized by digital clubbing, periostosis, and pachydermia. It is mainly caused by mutations in SLCO2A1 or HPGD, leading to impaired degradation and elevated levels of prostaglandin E2 (PGE2). In addition to the typical skeletal and skin manifestations, some patients may present with gastrointestinal or hematologic abnormalities, including anemia and myelofibrosis. This report describes a case of PHO with myelofibrosis and compound heterozygous SLCO2A1 mutations and review the literature. - Source: PubMed
Publication date: 2026/06/30
Xu QiruiLi QianLu JinWang Liru - The arachnoid mater-forming cells, which exhibit expressions of organic anion and cation transporters, as well as tight junction proteins, form the blood-arachnoid barrier. The purpose of the present study was to clarify the roles of the arachnoid mater transporters in the cerebrospinal fluid (CSF) clearance of prostaglandin D (PGD) and metformin by using an intracisternal administration method for evaluating arachnoid mater-mediated transport in rats. Global proteomics of rat leptomeninges showed the transporter expression of Slc22a6/Oat1, Slc22a8/Oat3, Slco2a1/Oatp2a1, Slc22a2/Oct2, and Slco2b1/Oatp2b1. The CSF clearance of PGD and metformin was greater than that of FITC-inulin, which is a marker of CSF bulk flow and parenchymal diffusion. The CSF elimination of PGD was significantly inhibited by p-aminohippuric acid, diclofenac (substrates/inhibitors of Slc22a6/Oat1 and Slc22a8/Oat3), and taurocholate (a broad substrate/inhibitor of Slco family transporters), whereas that of metformin was blocked by cimetidine, tetraethylammonium, and thiamine (substrates/inhibitors of Slc22a2/Oct2). The CSF-to-circulating blood transfer of metformin was inhibited by tetraethylammonium. These results suggested that the PGD clearance from the CSF most likely occurred via Slc22a6/Oat1, Slc22a8/Oat3, Slco2a1/Oatp2a1, and Slco2b1/Oatp2b1, while the metformin clearance was primarily mediated by Slc22a2/Oct2, in the arachnoid mater. These transporters would regulate the CSF concentrations of pharmacologically active substances and drugs. - Source: PubMed
Publication date: 2026/04/17
Yaguchi YukaSasaki KazunariInagaki MaiTerasaki TetsuyaTachikawa Masanori