Ask about this productRelated genes to: SLCO1A2 antibody
- Gene:
- SLCO1A2 NIH gene
- Name:
- solute carrier organic anion transporter family member 1A2
- Previous symbol:
- SLC21A3
- Synonyms:
- OATP, OATP1A2, OATP-A
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-05
- Date modifiied:
- 2016-10-05
Related products to: SLCO1A2 antibody
Related articles to: SLCO1A2 antibody
- Cerebrospinal fluid amyloid beta 42, total tau, and phosphorylated tau 181 are well accepted markers of Alzheimer's disease. These biomarkers better reflect disease pathogenesis compared to clinical diagnosis. Here, we perform a genome wide association study meta-analysis including 18,948 individuals of European ancestry and identify 12 genome-wide significant loci across all three biomarkers, eight of them novel. We replicate the association of biomarkers with APOE, CR1, GMNC/CCDC50 and C16orf95/MAP1LC3B. Novel loci include BIN1 for amyloid beta and GNA12, MS4A6A, SLCO1A2 with both total tau and phosphorylated tau 181, as well as additional loci on chr. 8, near ANGPT1 and chr. 9 near SMARCA2. We also demonstrate that these variants have significant association with Alzheimer's disease risk, disease progression and/or brain amyloidosis. The associated genes are implicated in lipid metabolism independent of APOE, coupled with autophagy and brain volume regulation driven by total tau and phosphorylated tau 181 dysregulation. - Source: PubMed
Publication date: 2026/04/21
Timsina JigyashaJiang ChenyangMcCartney Daniel LTao FeifeiDalmasso Maria CarolinaNajar JennaAnastasi FedericaOhlei OlenaPuerta Fuentes RaquelYang ChenyuBradley JosephWestern DanielAli MuhammadWang CiyangYang ChengranWu YingLiu MenghanBudde JohnWilliams JulieMahoney RebeccaCastillo Morales AtahualpaHohman Timothy JDumitrescu LoganWang Ting-ChenTesi Niccolo'Kern SilkeWaern MargdaSkoog Ingmarvan Harten ArgondePijnenburg Yolande A Lvan der Flier Wiesje MSánchez-Juan PascualRodriguez-Rodriguez EloyKleineidam LucaPeters OliverSchneider AnjaKüçükali FahriBellenguez CélineGrenier-Boley BenjaminHeikkinen Samide Rojas ItziarRujescu DanScherbaum NorbertHausner LucreziaDüzel EmrahGrimmer TimoWiltfang JensVandenberghe RikEngelborghs SebastiaanHeilmann-Heimbach StefanieSchmid MatthiasTegos ThomasScarmeas NikolaosDols-Icardo OriolMoreno FerminPérez-Tur JordiBullido María JSánchez-Valle RaquelÁlvarez VictoriaGarcía-González PabloMir PabloReal Luis MPiñol-Ripoll GerardGarcía-Alberca Jose MaríaSeelaar HarroRamakers InezPapma JanneHulsman MarcLaske ChristophTeipel StefanPriller JosefPerneczky RobertBuerger KatharinaNöthen Markus MLewczuk PiotrKornhuber JohannesHampel HaraldGiegling InaGoldhardt OliverDiehl-Schmid JanineAndrade VictorHeneka Michael MtFrölich LutzVogelgsang JonathanGraff CarolineThonberg HakanUllgren AbbePapenberg GoranDeleuze Jean-FrançoisDufouil CaroleWagner MichaelJessen FrankHolstege Hennevan Duijn CorneliaLebouvier ThibaudHannon OlivierLeinonen VilleSoininen HilkkaHerukka Sanna-KaisaGiedraitis VilmantasLöwenmark MalinKilander LenaGenius PatriciaRodríguez BlancaLuckett Emma SNavarro ArcadiCano AmandaMarquié MartaBlennow KajZetterberg HenrikLleo AlbertoBoada MercèRuiz AgustinLee Virginia Man-YeeVan Deerlin Vivianna MDeming YuetivaJohnson Sterling CEngelman Corinne DPastor PauAlvarez IgnacioPeskind Elaine RHeslegrave Amanda JSaykin Andrew JNho KwangsikSchindler Suzanne EMorris John CHoltzman David MMcDade EricRenton Alan EGoate AlisonIbanez LauraRiemenschneider MatthiasAlbert Marilyn SLaws Simon MPorter TenielleO'Brien Eleanor KShaw Leslie MTijms Betty MIngelsson MartinVisser Pieter JelleHiltunen MikkoSleegers KristelRitchie Craig WSims RebeccaBelloy MichaelLambert Jean-CharlesVilor-Tejedor NataliaFernández Maria VictoriaLi Qingqin SNagle Michael WMarioni Riccardo ERamirez AlfredoBertram Larsvan der Lee Sven JCruchaga Carlos - Esophageal cancer (EC) is a rapidly progressing malignancy that significantly contributes to cancer-related mortality. The genetic causes of EC, particularly rare coding pathogenic variants, remain incompletely defined. This study focuses on non-synonymous single nucleotide polymorphisms (nsSNPs) because they can impact the functions of critical proteins implicated in carcinogenesis. - Source: PubMed
Publication date: 2026/02/23
Azmi Muhammad BilalQureshi SajidaWasi RafiaNiaz Saad KhalidAhmed Syed Danish Haseen - The APOE-ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease. However, APOE-ε4 is not deterministic, highlighting the need to identify additional genetic and environmental factors. APOE-ε4 has been linked to accelerated cognitive decline, so we sought to investigate genetic factors that modify APOE-ε4-associated cognitive decline. We conduct cross-ancestry APOE-ε4-stratified and interaction GWAS using harmonized cognitive data from 32,778 participants, including 29,354 non-Hispanic White and 3,424 non-Hispanic Black individuals. Our primary outcome is late-life cognition, measured using harmonized composite scores for memory, executive function, and language, modeled as continuous traits reflecting both normative cognitive aging and disease-related decline. We identify two genome-wide significant loci in APOE-ε4 carriers, reaching genome-wide significance for executive function. These loci also demonstrate nominal associations across the other domains, suggesting broad effects on cognition. In non-carriers, we identify a genome-wide significant association at ITGB8 restricted to executive function, and another locus associated with language. We further link these loci to SEMA6D, GRIN3A, and ITGB8 through expression and methylation databases. Post-GWAS analyses implicate additional genes including SLCO1A2, and DNAH11. Genetic correlation analyses reveal differences by APOE-ε4 status for immune-related traits, suggesting immune-related predispositions may exacerbate cognitive risk in APOE-ε4 carriers. - Source: PubMed
Publication date: 2026/02/20
Contreras Alex GWalters SkylarEissman Jaclyn MArcher Derek BRegelson Alexandra NDurant AlainaClifton MichelleMukherjee SubhabrataLee Michael LChoi Seo-EunScollard PhoebeTrittschuh Emily HMez JesseBush William SKunkle Brian WCruchaga CarlosNaj Adam CGifford Katherine ABilgel MuratKuzma Amanda B Cuccaro Michael LPericak-Vance Margaret AFarrer Lindsay AWang Li-SanSchellenberg Gerard DHaines Jonathan LJefferson Angela LKukull Walter AKeene C DirkSaykin Andrew JThompson Paul MMartin Eden RAlbert Marilyn SJohnson Sterling CEngelman Corinne DFerrucci LuigiBennett David ABarnes Lisa LSchneider Julie ASperling Reisa AResnick Susan MCrane Paul KDumitrescu LoganHohman Timothy J - Gut microbiota, through both its species composition and its metabolites, impacts expression and activity of intestinal drug transporters. This phenomenon directly affects absorption process of orally administered drugs and contributes to the observed inter-individual variability in pharmacotherapeutic responses. This review summarizes mechanistic evidence from in vitro and animal studies and integrates clinical observations in which alterations in gut microbiota are associated with changes in oral drug exposure, consistent with potential regulation of key intestinal drug transporters-such as P-glycoprotein (P-gp, ABCB1), Breast Cancer Resistance Protein (BCRP, ABCG2), MRP2/3 proteins (ABCC2/3), and selected Organic Anion-Transporting Polypeptides (OATPs, e.g., SLCO1A2, SLCO2B1)-by major bacterial metabolites including short-chain fatty acids (SCFAs), secondary bile acids, and tryptophan-derived indoles. The molecular mechanisms involved include activation of nuclear and membrane receptors (PXR, FXR, AhR, TGR5), modulation of transcriptional and stress-response pathways (Nrf2, AP-1) with simultaneous suppression of pro-inflammatory pathways (NF-κB), and post-translational modifications (e.g., direct inhibition of P-gp ATPase activity by metabolites). The review also highlights the pharmacokinetic implications of, e.g., tacrolimus, digoxin, and metformin. In conclusion, the significance of "drug-transporter-microbiome" interactions for personalized medicine is discussed. Potential therapeutic interventions are also covered (diet, pre-/probiotics, fecal microbiota transplantation, modulation of PXR/FXR/AhR pathways). Considering the microbiota as a "second genome" enables more accurate prediction of drug exposure, reduction in toxicity, and optimization of dosing for orally administered preparations. - Source: PubMed
Publication date: 2025/12/10
Rzeczycki PatrykPęciak OliwiaPlust MartynaDroździk Marek - This study investigated the impact of genetic variations in organic anion transporting polypeptides (OATPs) 1A2 and 2B1 on their transport activity at pH 6.3 and 7.4 by using HEK293 cells expressing OATP variants, focusing on stoichiometric transport kinetic parameters corrected for the number of transporters on the plasma membrane. In the OATP2B1 Asp215Val, the maximal velocity per OATP molecule and intrinsic clearance at pH 6.3 were drastically reduced to 0.0648- and 0.0178-fold, respectively, compared with the wild type. All tested OATP1A2 variants exhibited increased transport activity at pH 6.3, suggesting that OATP1A2 is more sensitive to extracellular pH. Furthermore, we used the AlphaFold model to explain the observed differences in transport activity among genetic variants. In OATP1A2, the Glu172Asp mutation replaces a longer glutamate side chain with a shorter aspartate, which may enhance substrate interactions while weakening the salt-bridge interactions with neighboring residues, potentially compromising structural integrity. In OATP2B1, the Asp215Val variant was found to disrupt a key salt-bridge interaction with Lys595, which destabilizes the outward-open conformation. Moreover, the Val201Met mutation appears to lock the transporter in a single conformational state. Our findings underscore the importance of transmembrane helix 4 in maintaining functional conformational dynamics and suggest that mutations in this region can significantly alter substrate binding and transport efficiency in OATP1A2 and 2B1. SIGNIFICANCE STATEMENT: This study combined uptake assays using transporter-expressing cell lines, liquid chromatography-tandem mass spectrometry transporter quantification, and computer modeling to clarify the changes in transport activity per molecule, and these mechanisms caused by amino acid substitutions in organic anion transporting polypeptides 1A2 and 2B1. - Source: PubMed
Publication date: 2025/11/05
Akiyoshi TakeshiTonduru Arun KumarKataoka HirokiMorita TokioYajima KodaiImaoka AyukoKatayama KazuhiroMedarametla PrasanthiUchida YasuoPoso AnttiOhtani HisakazuTerasaki Tetsuya