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
- Fusobacterium nucleatum, a prevalent component of the intratumoral microbiome, has been associated with reduced survival in colorectal cancer. To enable sensitive and specific detection of F. nucleatum in tumor specimens, we developed a droplet digital PCR (ddPCR) assay targeting the transcription termination/anti-termination gene nusG, normalized to host tissue content using the solute carrier organic anion transporter family member 2A1 gene, SLCO2A1. Here, we present a ddPCR protocol optimized for quantifying F. nucleatum DNA in human genomic DNA extracted from formalin-fixed, paraffin-embedded (FFPE) tumor tissues. This methodology has been refined for high-throughput application, supporting large-scale analyses of F. nucleatum prevalence in tumor samples. - Source: PubMed
Kahsai OrsalemPhipps Amanda INewcomb Polly AHullar Meredith A J - - Source: PubMed
Publication date: 2026/08/17
Joshi ChitraDeme Justin CNakamura YoshinobuHsu Wei-TseGoult Jonathan DKato TakafumiParker Joanne LBiggin Philip CLea Susan MNakanishi TakeoNewstead Simon - 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