SLCO2A1
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Also known as PGTOATP2A1
Summary
SLCO2A1 (solute carrier organic anion transporter family member 2A1, HGNC:10955) is a protein-coding gene on chromosome 3q22.1-q22.2, encoding Solute carrier organic anion transporter family member 2A1 (Q92959). Mediates the transport of prostaglandins (PGs, mainly PGE2, PGE1, PGE3, PGF2alpha, PGD2, PGH2) and thromboxanes (thromboxane B2) across the cell membrane.
This gene encodes a prostaglandin transporter that is a member of the 12-membrane-spanning superfamily of transporters. The encoded protein may be involved in mediating the uptake and clearance of prostaglandins in numerous tissues.
Source: NCBI Gene 6578 — RefSeq curated summary.
At a glance
- Gene–disease (curated): hypertrophic osteoarthropathy, primary, autosomal dominant (Definitive, GenCC) — +4 more curated relationships
- GWAS associations: 3
- Clinical variants (ClinVar): 363 total — 37 pathogenic, 21 likely-pathogenic
- Phenotypes (HPO): 54
- Druggable target: yes — 1 molecules with ChEMBL bioactivity
- MANE Select transcript:
NM_005630
Identifiers
Gene identifiers
| Field | Value |
|---|---|
| HGNC ID | HGNC:10955 |
| Approved symbol | SLCO2A1 |
| Name | solute carrier organic anion transporter family member 2A1 |
| Location | 3q22.1-q22.2 |
| Locus type | gene with protein product |
| Status | Approved |
| Aliases | PGT, OATP2A1 |
| Ensembl gene | ENSG00000174640 |
| Ensembl biotype | protein_coding |
| OMIM | 601460 |
| Entrez | 6578 |
Gene structure
Transcript identifiers
Ensembl transcripts: 17 — 11 protein_coding, 3 retained_intron, 2 protein_coding_CDS_not_defined, 1 nonsense_mediated_decay
ENST00000310926, ENST00000462770, ENST00000464676, ENST00000477061, ENST00000478651, ENST00000478662, ENST00000481359, ENST00000493729, ENST00000860067, ENST00000860068, ENST00000860069, ENST00000860070, ENST00000860071, ENST00000860072, ENST00000860073, ENST00000860074, ENST00000860075
RefSeq mRNA: 1 — MANE Select: NM_005630
NM_005630
CCDS: CCDS3084
Canonical transcript exons
ENST00000310926 — 14 exons
| Exon | Start | End |
|---|---|---|
| ENSE00001184806 | 133948893 | 133948971 |
| ENSE00001184828 | 133932701 | 133934830 |
| ENSE00001250528 | 134029707 | 134029925 |
| ENSE00001305936 | 133951208 | 133951344 |
| ENSE00003531773 | 133979481 | 133979618 |
| ENSE00003541500 | 133945095 | 133945260 |
| ENSE00003581552 | 133947256 | 133947445 |
| ENSE00003599910 | 133973663 | 133973825 |
| ENSE00003601676 | 133953663 | 133953761 |
| ENSE00003617669 | 133954966 | 133955193 |
| ENSE00003618950 | 133935774 | 133935897 |
| ENSE00003622918 | 133948536 | 133948700 |
| ENSE00003644863 | 133942605 | 133942768 |
| ENSE00003657886 | 133938429 | 133938493 |
Expression profiles
Bgee: expression breadth ubiquitous, 252 present calls, max score 99.40.
FANTOM5 (CAGE): breadth broad, TPM avg 6.1463 / max 585.1530, expressed in 641 samples.
FANTOM5 promoters (5 alternative TSS)
| Promoter ID | TPM avg | Samples expressed |
|---|---|---|
| 44681 | 5.0564 | 561 |
| 44682 | 0.6154 | 267 |
| 44683 | 0.2787 | 135 |
| 44684 | 0.1410 | 70 |
| 44677 | 0.0549 | 23 |
Top tissues by expression
289 total, by Bgee expression score (0-100, higher = more expressed):
| Tissue | Anatomy ID | Expression score | Quality |
|---|---|---|---|
| right lung | UBERON:0002167 | 99.40 | gold quality |
| upper lobe of left lung | UBERON:0008952 | 97.97 | gold quality |
| upper lobe of lung | UBERON:0008948 | 97.87 | gold quality |
| right lobe of thyroid gland | UBERON:0001119 | 97.77 | gold quality |
| left lobe of thyroid gland | UBERON:0001120 | 97.35 | gold quality |
| thyroid gland | UBERON:0002046 | 96.91 | gold quality |
| lower lobe of lung | UBERON:0008949 | 96.53 | gold quality |
| seminal vesicle | UBERON:0000998 | 96.33 | gold quality |
| lung | UBERON:0002048 | 94.85 | gold quality |
| cardia of stomach | UBERON:0001162 | 94.10 | gold quality |
| left uterine tube | UBERON:0001303 | 94.04 | gold quality |
| mucosa of stomach | UBERON:0001199 | 93.42 | gold quality |
| body of uterus | UBERON:0009853 | 93.28 | gold quality |
| left adrenal gland cortex | UBERON:0035825 | 93.26 | gold quality |
| adrenal cortex | UBERON:0001235 | 93.19 | gold quality |
| left adrenal gland | UBERON:0001234 | 93.11 | gold quality |
| decidua | UBERON:0002450 | 92.84 | gold quality |
| tendon of biceps brachii | UBERON:0008188 | 92.73 | gold quality |
| right adrenal gland | UBERON:0001233 | 92.55 | gold quality |
| myometrium | UBERON:0001296 | 92.55 | gold quality |
| right adrenal gland cortex | UBERON:0035827 | 92.46 | gold quality |
| ectocervix | UBERON:0012249 | 91.96 | gold quality |
| smooth muscle tissue | UBERON:0001135 | 91.81 | gold quality |
| adrenal gland | UBERON:0002369 | 91.50 | gold quality |
| right coronary artery | UBERON:0001625 | 91.07 | gold quality |
| pylorus | UBERON:0001166 | 90.71 | gold quality |
| left coronary artery | UBERON:0001626 | 90.47 | gold quality |
| fundus of stomach | UBERON:0001160 | 90.34 | gold quality |
| palpebral conjunctiva | UBERON:0001812 | 90.33 | gold quality |
| gall bladder | UBERON:0002110 | 90.23 | gold quality |
Single-cell (SCXA)
Detected in 9 experiment(s), a significant marker in 8.
| Experiment | Marker? | Max mean expression |
|---|---|---|
| E-ANND-2 | yes | 713.61 |
| E-GEOD-135922 | yes | 636.52 |
| E-HCAD-11 | yes | 42.76 |
| E-CURD-119 | yes | 40.43 |
| E-HCAD-1 | yes | 39.28 |
| E-MTAB-8410 | yes | 22.10 |
| E-MTAB-6678 | yes | 6.33 |
| E-MTAB-10137 | no | 515.82 |
| E-ANND-3 | no | 0.00 |
Regulation
Is transcription factor: no
miRNA regulators (miRDB)
88 targeting SLCO2A1, top 30 by miRDB confidence (max_score; target_count = how many genes the miRNA targets in total — lower means more specific):
| miRNA | Max score | Avg score | miRNA target_count |
|---|---|---|---|
| HSA-MIR-7110-3P | 100.00 | 73.18 | 2486 |
| HSA-MIR-6833-3P | 100.00 | 70.63 | 3197 |
| HSA-MIR-6740-5P | 100.00 | 65.64 | 932 |
| HSA-MIR-34A-5P | 99.99 | 71.21 | 1784 |
| HSA-MIR-449A | 99.99 | 71.05 | 1776 |
| HSA-MIR-3667-3P | 99.99 | 67.17 | 1636 |
| HSA-MIR-548P | 99.98 | 72.25 | 3784 |
| HSA-MIR-3692-3P | 99.98 | 70.27 | 2139 |
| HSA-MIR-34C-5P | 99.97 | 70.45 | 1577 |
| HSA-MIR-449B-5P | 99.97 | 70.26 | 1580 |
| HSA-MIR-6825-5P | 99.96 | 69.81 | 3431 |
| HSA-MIR-1468-3P | 99.96 | 72.74 | 3797 |
| HSA-MIR-3143 | 99.93 | 71.96 | 3104 |
| HSA-MIR-3119 | 99.92 | 71.34 | 2390 |
| HSA-MIR-6780A-5P | 99.88 | 66.69 | 2776 |
| HSA-MIR-605-3P | 99.88 | 69.22 | 1833 |
| HSA-MIR-4728-5P | 99.85 | 69.39 | 4718 |
| HSA-MIR-6785-5P | 99.82 | 68.68 | 4428 |
| HSA-MIR-6817-3P | 99.79 | 68.35 | 2126 |
| HSA-MIR-1273H-5P | 99.77 | 66.32 | 2471 |
| HSA-MIR-6763-5P | 99.76 | 64.68 | 1767 |
| HSA-MIR-149-3P | 99.72 | 68.22 | 3963 |
| HSA-MIR-1200 | 99.71 | 70.42 | 1838 |
| HSA-MIR-30B-3P | 99.70 | 65.76 | 2325 |
| HSA-MIR-3689A-3P | 99.70 | 65.73 | 2306 |
| HSA-MIR-3689B-3P | 99.70 | 65.71 | 2311 |
| HSA-MIR-3689C | 99.70 | 65.71 | 2311 |
| HSA-MIR-6779-5P | 99.70 | 65.76 | 2363 |
| HSA-MIR-6883-5P | 99.69 | 68.05 | 3785 |
| HSA-MIR-5093 | 99.67 | 69.26 | 2291 |
Literature-anchored findings (GeneRIF, showing 40)
- Human endometrial stromal cells treated with a combination of cAMP and medroxyprogesterone acetate to induce decidualization showed an increase in protein and mRNA levels. (PMID:16339169)
- PGT level was significantly less in AD than in age-matched control brain homogenates. (PMID:18353443)
- The existing model to explain increased PGE(2) in colorectal neoplasia should be modified to include the novel mechanism of coordinated up- and down-regulation of genes involved in PGE(2) transport. (PMID:19138942)
- that PGT may play a role in transporting PGH(2) across cellular membranes. (PMID:20346915)
- expression in fetal membranesfound primarily in the choriodecidua (PMID:20357271)
- we found no indication for an association between SNPs in the prostaglandin F(2alpha) receptor gene or SLCO2A1 and IOP response to prostaglandin analogs in a population of European descent. (PMID:22060278)
- The findings confirmed that SLCO2A1 mutations inactivate prostaglandin E2 transport, and they indicated that mutations in SLCO2A1 are the pathogenic cause of primary hypertrophic osteoarthropathy. (PMID:22197487)
- Mutations in the prostaglandin transporter encoding gene SLCO2A1 cause primary hypertrophic osteoarthropathy and isolated digital clubbing. (PMID:22331663)
- Prostaglandin transporter mutations cause pachydermoperiostosis with myelofibrosis. (PMID:22553128)
- Mutations in the prostaglandin transporter SLCO2A1 cause primary hypertrophic osteoarthropathy with digital clubbing. (PMID:22696055)
- Report SLCO2A1 is a novel gene responsible for pachydermoperiostosis in Japanese patients. (PMID:22906430)
- genetic association study in population in China: Nine different SLCO2A1 mutations were identified in subjects with primary hypertrophic osteoarthropathy (PHO) in 7 previously undescribed families; different homozygous mutations of SLCO2A1 cause PHO. (PMID:23509104)
- Three novel mutations within the SLCO2A1 gene have been demonstrated to be associated with Chinese primary hypertrophic osteoarthropathy patients. (PMID:24153155)
- Identified two novel mutations in SLCO2A1. (PMID:24185079)
- Genetic variability in key genes in prostaglandin E2 pathway (COX-2, HPGD, ABCC4 and SLCO2A1) and their involvement in colorectal cancer development. (PMID:24694755)
- SLCO2A1 has a role in familial digital clubbing, colon neoplasia, and NSAID resistance (PMID:24838973)
- a novel nonsense mutation p.E141* of the SLCO2A1 gene is associated with pachydermoperiostosis (PMID:24929850)
- In this article we describe a novel mutation in the SLCO2A1 causing Pachydermoperiostosis in a Lebanese family (PMID:25059581)
- OATP2A1 also diminished the PGE2-mediated expression of interleukin-8 mRNA (IL-8) and hypoxia-inducible-factor 1alpha (HIF1alpha) protein in AGS-OATP2A1 cells. (PMID:25433165)
- Multiple drug resistance-associated protein 4 (MRP4), prostaglandin transporter (PGT), and 15-hydroxyprostaglandin dehydrogenase (15-PGDH) as determinants of PGE2 levels in cancer. (PMID:25433169)
- We herein report patients with pachydermoperiostosis (PDP)due to SLCO2A1 mutation in a Korean family. Similar to other East Asian populations, the SLCO2A1 gene may be a possible mutation spot of PDP in the Korean population. (PMID:25810087)
- SLCO2A1 and NOS3 are involved with prostaglandin reuptake/metabolism and nitric oxide production, respectively, and are consistently decreased in “non-Caucasian” fetal ductus arteriosus (PMID:26265282)
- overexpression of SLCO2A1 could induce and knockdown inhibit the invasion of lung cancer cells. expression levels of p-mTOR, p-AKT and p-S6 were up-regulated or down-regulated with the overexpression or knockdown of SLCO2A1. (PMID:26464663)
- findings indicate that loss-of-function mutations in the SLCO2A1 gene encoding a prostaglandin transporter cause the hereditary enteropathy CNSU (PMID:26539716)
- Data show that prostaglandin E3 (PGE3) uptake by prostaglandin transporter OATP2A1-expressing HEK293 cells (HEK/2A1) was the highest and followed by SLCO2B1 (HEK/1B1). (PMID:26692285)
- cytoplasmic OATP2A1 likely facilitates prostaglandin E2 loading into suitable intracellular compartment(s) for efficient exocytotic prostaglandin E2 release from colorectal cancer cells exposed to oxidative stress (PMID:26850138)
- Mutation analysis revealed a novel heterozygous mutation in the solute carrier organic anion transporter family member 2A1 gene at nucleotide 302 causing a substitution of the amino acid isoleucine to serine at codon 101 (p.IIe101Ser) in affected individuals. (PMID:27134495)
- An association was found between single nucleotide polymorphisms of the PTGFR and SLCO2A1 genes and the response to latanoprost in Han Chinese patients with glaucoma. These SNPs may be important determinants of differential response to latanoprost. (PMID:27336732)
- In Japanese patients with chronic nonspecific multiple ulcers of the small intestine, 2 of the 4 patients had mutation in the SLCO2A1 gene, became resistant to medical therapy, and underwent strictureplasty or ileal resection after long-term follow-up. (PMID:27467110)
- The findings reported here support causality of this SLCO2A1 mutation for autosomal recessive ICNC in this consanguineous Pakistani kindred. (PMID:27681482)
- A novel missense mutation c.101T > C in the SLCO2A1 gene causes pachydermoperiostosis of the complete type. (PMID:28602931)
- in individuals carrying the SLCO2A1 A396T variant, the combination of thiazide-specific effects on free water generation and the increase in collecting duct water permeability from reduced SLCO2A1 activity combine to produce thiazide-induced hyponatremia (PMID:28783044)
- The expression of SLCO2A1 was observed in one of four patients with chronic enteropathy associated with SLCO2A1 (CEAS) and in all 29 patients with Crohn’s Disease. The three with CEAS without SLCO2A1 expression had a homozygous splice-site mutation in SLCO2A1. The remaining one CEAS patient with positive expression of SLCO2A1 had compound heterozygous mutations. (PMID:30400730)
- A novel SLCO2A1 compound heterozygous mutation of p.I284V and p.C459R was identified in two PHO patients in a chinese family. (PMID:31004291)
- Chronic enteropathy associated with SLCO2A1 gene: A case report and literature review. (PMID:31196708)
- A novel mutation in the SLCO2A1 gene, encoding a prostaglandin transporter, induces chronic enteropathy. (PMID:33166338)
- [Clinical and genetic characteristics of patients with chronic enteropathy associated with SLCO2A1 gene]. (PMID:33397021)
- Differential Associations of SLCO Transporters with Prostate Cancer Aggressiveness between African Americans and European Americans. (PMID:33619025)
- Phenolsulfonphthalein as a surrogate substrate to assess altered function of the prostaglandin transporter SLCO2A1. (PMID:35299026)
- Clinical and Genetic Characteristics of Korean Patients Diagnosed with Chronic Enteropathy Associated with SLCO2A1 Gene: A KASID Multicenter Study. (PMID:35611666)
Cross-species orthologs
4 orthologs
| Organism | Symbol | Gene ID |
|---|---|---|
| danio_rerio | slco2a1 | ENSDARG00000061896 |
| mus_musculus | Slco2a1 | ENSMUSG00000032548 |
| rattus_norvegicus | Slco2a1 | ENSRNOG00000009005 |
| drosophila_melanogaster | Oatp30B | FBGN0032123 |
Paralogs (10): SLCO1A2 (ENSG00000084453), SLCO4A1 (ENSG00000101187), SLCO1B3 (ENSG00000111700), SLCO1B1 (ENSG00000134538), SLCO2B1 (ENSG00000137491), SLCO5A1 (ENSG00000137571), SLCO1C1 (ENSG00000139155), SLCO4C1 (ENSG00000173930), SLCO3A1 (ENSG00000176463), SLCO6A1 (ENSG00000205359)
Protein
Protein identifiers
Solute carrier organic anion transporter family member 2A1 — Q92959 (reviewed: Q92959)
Alternative names: OATP2A1, PHOAR2, Prostaglandin transporter, Solute carrier family 21 member 2
All UniProt accessions (3): E7EU40, Q92959, F8W9W8
UniProt curated annotations — full annotation on UniProt →
Function. Mediates the transport of prostaglandins (PGs, mainly PGE2, PGE1, PGE3, PGF2alpha, PGD2, PGH2) and thromboxanes (thromboxane B2) across the cell membrane. PGs and thromboxanes play fundamental roles in diverse functions such as intraocular pressure, gastric acid secretion, renal salt and water transport, vascular tone, and fever. Plays a role in the clearance of PGs from the circulation through cellular uptake, which allows cytoplasmic oxidation and PG signal termination. PG uptake is dependent upon membrane potential and involves exchange of a monovalent anionic substrate (PGs exist physiologically as an anionic monovalent form) with a stoichiometry of 1:1 for divalent anions or of 1:2 for monovalent anions. Uses lactate, generated by glycolysis, as a counter-substrate to mediate PGE2 influx and efflux. Under nonglycolytic conditions, metabolites other than lactate might serve as counter-substrates. Although the mechanism is not clear, this transporter can function in bidirectional mode. When apically expressed in epithelial cells, it facilitates transcellular transport (also called vectorial release), extracting PG from the apical medium and facilitating transport across the cell toward the basolateral side, whereupon the PG exits the cell by simple diffusion. In the renal collecting duct, regulates renal Na+ balance by removing PGE2 from apical medium (PGE2 EP4 receptor is likely localized to the luminal/apical membrane and stimulates Na+ resorption) and transporting it toward the basolateral membrane (where PGE2 EP1 and EP3 receptors inhibit Na+ resorption). Plays a role in endometrium during decidualization, increasing uptake of PGs by decidual cells. Involved in critical events for ovulation. Regulates extracellular PGE2 concentration for follicular development in the ovaries. Expressed intracellularly, may contribute to vesicular uptake of newly synthesized intracellular PGs, thereby facilitating exocytotic secretion of PGs without being metabolized. Essential core component of the major type of large-conductance anion channel, Maxi-Cl, which plays essential roles in inorganic anion transport, cell volume regulation and release of ATP and glutamate not only in physiological processes but also in pathological processes. May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier.
Subcellular location. Cell membrane. Basal cell membrane. Cytoplasm. Lysosome.
Tissue specificity. Ubiquitous. Significant expression observed in lung, kidney, spleen, and heart. Expressed in the endometrium (at both mRNA and protein levels). Expressed in the ovaries (at mRNA and protein levels). In testis, primarily localized to the basal membrane of Sertoli cells and weakly expressed within the tubules.
Disease relevance. PHOAR2-enteropathy syndrome (PHOAR2E) [MIM:614441] An autosomal recessive disease characterized by primary hypertrophic osteoarthropathy and/or chronic non-specific ulcers of the small intestine. Affected individuals present with digital clubbing, periostosis, acroosteolysis, painful joint enlargement, and variable features of pachydermia that include thickened facial skin and a thickened scalp. Chronic ulcers of the small intestine result in abdominal pain and watery diarrhea, and are associated with chronic anemia. Other developmental anomalies include delayed closure of the cranial sutures and congenital heart disease. The disease is caused by variants affecting the gene represented in this entry. Hypertrophic osteoarthropathy, primary, autosomal dominant (PHOAD) [MIM:167100] A form of primary hypertrophic osteoarthropathy, a disease characterized by digital clubbing, periostosis, acroosteolysis, painful joint enlargement, and variable features of pachydermia that include thickened facial skin and a thickened scalp. PHOAD patients may also experience joint swelling and pain, and some have reported gastrointestinal symptoms, including watery diarrhea. Males are more commonly affected, and more severely affected, than females. The disease is caused by variants affecting the gene represented in this entry.
Activity regulation. Chorionic gonadotropin stimulates expression in the ovaries.
Similarity. Belongs to the organo anion transporter (TC 2.A.60) family.
RefSeq proteins (1): NP_005621* (*=MANE)
Domains & families (InterPro)
| ID | Name | Type |
|---|---|---|
| IPR002350 | Kazal_dom | Domain |
| IPR004156 | OATP | Family |
| IPR020846 | MFS_dom | Domain |
| IPR036058 | Kazal_dom_sf | Homologous_superfamily |
| IPR036259 | MFS_trans_sf | Homologous_superfamily |
Pfam: PF03137, PF07648
Catalyzed reactions (Rhea), 8 shown:
- prostaglandin E2(out) = prostaglandin E2(in) (RHEA:50984)
- prostaglandin E3(out) + 2 (S)-lactate(in) = prostaglandin E3(in) + 2 (S)-lactate(out) (RHEA:74351)
- prostaglandin H2(out) + 2 (S)-lactate(in) = prostaglandin H2(in) + 2 (S)-lactate(out) (RHEA:74379)
- prostaglandin E2(out) + 2 (S)-lactate(in) = prostaglandin E2(in) + 2 (S)-lactate(out) (RHEA:74383)
- prostaglandin E1(out) + 2 (S)-lactate(in) = prostaglandin E1(in) + 2 (S)-lactate(out) (RHEA:74395)
- prostaglandin F2alpha(out) + 2 (S)-lactate(in) = prostaglandin F2alpha(in) + 2 (S)-lactate(out) (RHEA:74399)
- prostaglandin D2(out) + 2 (S)-lactate(in) = prostaglandin D2(in) + 2 (S)-lactate(out) (RHEA:74403)
- thromboxane B2(out) + 2 (S)-lactate(in) = thromboxane B2(in) + 2 (S)-lactate(out) (RHEA:74407)
UniProt features (113 total): helix 30, sequence variant 24, strand 14, topological domain 13, transmembrane region 12, turn 10, glycosylation site 3, disulfide bond 3, sequence conflict 2, chain 1, domain 1
Structure
Experimental structures (PDB)
7 structures.
| PDB | Method | Resolution (Å) |
|---|---|---|
| 3MRR | X-RAY DIFFRACTION | 1.6 |
| 8KGW | ELECTRON MICROSCOPY | 2.96 |
| 9JV1 | ELECTRON MICROSCOPY | 3.1 |
| 8KGI | ELECTRON MICROSCOPY | 3.2 |
| 8KGV | ELECTRON MICROSCOPY | 3.2 |
| 9JUQ | ELECTRON MICROSCOPY | 3.2 |
| 9MGK | ELECTRON MICROSCOPY | 4.3 |
Predicted structure (AlphaFold)
| Model | pLDDT | Fraction very-high |
|---|---|---|
| AF-Q92959-F1 | 82.27 | 0.48 |
Functional residue map
Curated UniProt residues grouped by drug-discovery relevance — catalytic, ligand-binding, modification, and mutation-validated positions. Source: UniProtKB sequence features.
Disulfide bonds (3): 444–474, 450–470, 459–494
Glycosylation sites (3): 134, 478, 491
Function
Pathways and Gene Ontology
Reactome pathways
8 pathways
| ID | Pathway |
|---|---|
| R-HSA-5619095 | Defective SLCO2A1 causes primary, autosomal recessive hypertrophic osteoarthropathy 2 (PHOAR2) |
| R-HSA-879518 | Organic anion transport by SLCO transporters |
| R-HSA-1643685 | Disease |
| R-HSA-382551 | Transport of small molecules |
| R-HSA-425397 | Transport of vitamins, nucleosides, and related molecules |
| R-HSA-425407 | SLC-mediated transmembrane transport |
| R-HSA-5619102 | SLC transporter disorders |
| R-HSA-5619115 | Disorders of transmembrane transporters |
MSigDB gene sets: 294 (showing top):
GSE45365_NK_CELL_VS_BCELL_UP, GOBP_SODIUM_INDEPENDENT_ORGANIC_ANION_TRANSPORT, BENPORATH_ES_WITH_H3K27ME3, TGACCTY_ERR1_Q2, SAENZ_DETOX_PATHWAY_AND_CARCINOGENESIS_DN, GOBP_ORGANIC_ACID_TRANSPORT, BROWNE_HCMV_INFECTION_48HR_DN, HOSHIDA_LIVER_CANCER_SUBCLASS_S3, ROZANOV_MMP14_TARGETS_UP, NF1_Q6_01, KYNG_DNA_DAMAGE_BY_GAMMA_RADIATION, SCHAEFFER_PROSTATE_DEVELOPMENT_48HR_UP, GOBP_ORGANIC_ANION_TRANSPORT, MORF_EPHA7, GOBP_MONOCARBOXYLIC_ACID_TRANSPORT
GO Biological Process (5): lipid transport (GO:0006869), prostaglandin transport (GO:0015732), sodium-independent organic anion transport (GO:0043252), monoatomic ion transport (GO:0006811), transmembrane transport (GO:0055085)
GO Molecular Function (5): lipid carrier activity (GO:0005319), prostaglandin transmembrane transporter activity (GO:0015132), obsolete sodium-independent organic anion transmembrane transporter activity (GO:0015347), protein binding (GO:0005515), transmembrane transporter activity (GO:0022857)
GO Cellular Component (6): lysosome (GO:0005764), plasma membrane (GO:0005886), basal plasma membrane (GO:0009925), membrane (GO:0016020), basolateral plasma membrane (GO:0016323), cytoplasm (GO:0005737)
Reactome top-level categories
Rollup of top-6 pathways:
| Category | Pathways |
|---|---|
| SLC transporter disorders | 1 |
| SLC-mediated transport of organic anions | 1 |
| SLC-mediated transmembrane transport | 1 |
| Transport of small molecules | 1 |
| Disorders of transmembrane transporters | 1 |
| Disease | 1 |
GO top-level categories
Rollup of top GO terms by namespace:
| Category | Terms |
|---|---|
| transport | 3 |
| transmembrane transport | 2 |
| plasma membrane region | 2 |
| cellular anatomical structure | 2 |
| lipid localization | 1 |
| fatty acid transport | 1 |
| icosanoid transport | 1 |
| cellular process | 1 |
| molecular carrier activity | 1 |
| prostaglandin transport | 1 |
| icosanoid transmembrane transporter activity | 1 |
| binding | 1 |
| transporter activity | 1 |
| lytic vacuole | 1 |
| membrane | 1 |
| cell periphery | 1 |
| basal part of cell | 1 |
| basal plasma membrane | 1 |
| intracellular anatomical structure | 1 |
Protein interactions and networks
STRING
1114 interactions, top by confidence (×1000):
| Protein A | Protein B | Partner UniProt | Score |
|---|---|---|---|
| SLCO2A1 | ITIH4 | Q14624 | 877 |
| SLCO2A1 | HPGD | P15428 | 766 |
| SLCO2A1 | ABCC4 | O15439 | 596 |
| SLCO2A1 | MAN1A1 | P33908 | 591 |
| SLCO2A1 | AMH | P03971 | 588 |
| SLCO2A1 | PTGFR | P43088 | 543 |
| SLCO2A1 | PTGER2 | P43116 | 537 |
| SLCO2A1 | PTGER4 | P35408 | 526 |
| SLCO2A1 | PTGES | O14684 | 512 |
| SLCO2A1 | PTGER3 | P43115 | 454 |
| SLCO2A1 | PPARG | P37231 | 451 |
| SLCO2A1 | ABCB1 | P08183 | 449 |
| SLCO2A1 | GNRH1 | P01148 | 447 |
| SLCO2A1 | NR1I2 | O75469 | 435 |
| SLCO2A1 | SLC22A8 | Q8TCC7 | 429 |
IntAct
3 interactions, top by confidence:
| A | B | Type | Score |
|---|---|---|---|
| SLCO2A1 | GRB2 | psi-mi:“MI:0915”(physical association) | 0.400 |
| SLCO2A1 | ATP5PD | psi-mi:“MI:0914”(association) | 0.350 |
BioGRID (6): ACBD3 (Affinity Capture-MS), ATP5D (Affinity Capture-MS), ATP5H (Affinity Capture-MS), PLD3 (Affinity Capture-MS), RDH14 (Affinity Capture-MS), TMX1 (Affinity Capture-MS)
ESM2 similar proteins: A1L1W9, A1L272, A2SWM2, A8WGF7, D3Z5L6, D4A9K4, F4IKF6, G5E8K6, G8XYX6, O15374, O35440, O70324, O70451, O70594, P30638, P36021, P53985, P53986, P53987, P53988, P57057, P58355, Q00910, Q03064, Q0VA82, Q3MHW6, Q3U9N9, Q569T7, Q5M7K3, Q5U3U7, Q5XGK0, Q63344, Q640L2, Q6DCX5, Q6GPQ3, Q6NMN6, Q6NT16, Q6NUB3, Q7ZWG6, Q8AVC3
Diamond homologs: F5H094, G3V0H7, O35913, O88397, O94956, P46720, P46721, P70502, Q00910, Q5RFF0, Q6ZQN7, Q71MB6, Q8BGD4, Q8BXB6, Q8HYW2, Q8R3L5, Q91YY5, Q92959, Q96BD0, Q99J94, Q99N01, Q99N02, Q9EP96, Q9EPT5, Q9EPZ7, Q9ERB5, Q9GMU6, Q9H2Y9, Q9JHI3, Q9JJL3, Q9NPD5, Q9NYB5, Q9QXZ6, Q9QYE2, Q9QZX8, Q9UIG8, Q9Y6L6, Q8K078, Q86UG4, Q8C0X7
SIGNOR signaling
0 interactions.
Disease & clinical
Clinical variants and AI predictions
ClinVar
363 variants total. Per-class counts are floors (≥ shown; pagination cap):
| Classification | Count (floor) |
|---|---|
| Pathogenic | 37 |
| Likely pathogenic | 21 |
| Uncertain significance | 119 |
| Likely benign | 117 |
| Benign | 39 |
Top pathogenic / likely-pathogenic (30)
| Variant ID | HGVS | Classification |
|---|---|---|
| 1174120 | NM_005630.3(SLCO2A1):c.861+2T>C | Pathogenic |
| 1174121 | NM_005630.3(SLCO2A1):c.302T>G (p.Ile101Ser) | Pathogenic |
| 1174123 | NM_005630.3(SLCO2A1):c.621C>A (p.Tyr207Ter) | Pathogenic |
| 1174124 | NM_005630.3(SLCO2A1):c.1660G>A (p.Gly554Arg) | Pathogenic |
| 1174125 | NM_005630.3(SLCO2A1):c.1814+1G>A | Pathogenic |
| 1350810 | NM_005630.3(SLCO2A1):c.310G>A (p.Gly104Arg) | Pathogenic |
| 1363789 | NM_005630.3(SLCO2A1):c.1264_1265del (p.Thr422fs) | Pathogenic |
| 1483488 | NM_005630.3(SLCO2A1):c.1106G>A (p.Gly369Asp) | Pathogenic |
| 1978090 | NM_005630.3(SLCO2A1):c.1768del (p.Arg590fs) | Pathogenic |
| 225478 | NM_005630.3(SLCO2A1):c.940+1G>A | Pathogenic |
| 2708031 | NM_005630.3(SLCO2A1):c.1497dup (p.Ala500fs) | Pathogenic |
| 2920730 | NM_005630.3(SLCO2A1):c.421G>T (p.Glu141Ter) | Pathogenic |
| 2920732 | NM_005630.3(SLCO2A1):c.1106-1G>A | Pathogenic |
| 2920734 | NM_005630.3(SLCO2A1):c.178G>A (p.Glu60Lys) | Pathogenic |
| 2920736 | NM_005630.3(SLCO2A1):c.759G>A (p.Trp253Ter) | Pathogenic |
| 2920737 | NM_005630.3(SLCO2A1):c.440G>A (p.Trp147Ter) | Pathogenic |
| 2920740 | NM_005630.3(SLCO2A1):c.1095C>A (p.Asn365Lys) | Pathogenic |
| 2920742 | NM_005630.3(SLCO2A1):c.1668G>C (p.Gln556His) | Pathogenic |
| 2920743 | NM_005630.3(SLCO2A1):c.763G>A (p.Gly255Arg) | Pathogenic |
| 2920744 | NM_005630.3(SLCO2A1):c.855del (p.Ala286fs) | Pathogenic |
| 2920745 | NM_005630.3(SLCO2A1):c.1461+1G>C | Pathogenic |
| 3016178 | NM_005630.3(SLCO2A1):c.794del (p.Ser264_Ser265insTer) | Pathogenic |
| 30186 | NM_005630.3(SLCO2A1):c.97-1G>A | Pathogenic |
| 30187 | NM_005630.3(SLCO2A1):c.764G>A (p.Gly255Glu) | Pathogenic |
| 30188 | NM_005630.3(SLCO2A1):c.1634del (p.Asn545fs) | Pathogenic |
| 3068564 | NM_005630.3(SLCO2A1):c.209_210insA (p.Leu72fs) | Pathogenic |
| 3688289 | NM_005630.3(SLCO2A1):c.1183C>T (p.Gln395Ter) | Pathogenic |
| 3696256 | NM_005630.3(SLCO2A1):c.1022del (p.Val341fs) | Pathogenic |
| 37167 | NM_005630.3(SLCO2A1):c.830dup (p.Phe278fs) | Pathogenic |
| 37168 | NM_005630.3(SLCO2A1):c.754C>T (p.Arg252Ter) | Pathogenic |
SpliceAI
2991 predictions. Top by Δscore:
| Variant | Effect | Δscore |
|---|---|---|
| 3:133934829:ACCT:A | acceptor_loss | 1.0000 |
| 3:133934831:C:CG | acceptor_loss | 1.0000 |
| 3:133934832:T:C | acceptor_loss | 1.0000 |
| 3:133935768:CCTCA:C | donor_loss | 1.0000 |
| 3:133935769:CTCAC:C | donor_loss | 1.0000 |
| 3:133935770:TCA:T | donor_loss | 1.0000 |
| 3:133935771:CA:C | donor_loss | 1.0000 |
| 3:133935773:C:G | donor_loss | 1.0000 |
| 3:133935773:CCTGT:C | donor_gain | 1.0000 |
| 3:133938422:CACTT:C | donor_loss | 1.0000 |
| 3:133938423:ACTT:A | donor_loss | 1.0000 |
| 3:133938424:CTTA:C | donor_loss | 1.0000 |
| 3:133938425:TTAC:T | donor_loss | 1.0000 |
| 3:133938426:TAC:T | donor_loss | 1.0000 |
| 3:133938427:A:AC | donor_gain | 1.0000 |
| 3:133938427:AC:A | donor_gain | 1.0000 |
| 3:133938427:ACCCA:A | donor_loss | 1.0000 |
| 3:133938428:C:CC | donor_gain | 1.0000 |
| 3:133938428:CC:C | donor_gain | 1.0000 |
| 3:133938428:CCCAG:C | donor_gain | 1.0000 |
| 3:133938489:CCACA:C | acceptor_gain | 1.0000 |
| 3:133938490:CACA:C | acceptor_gain | 1.0000 |
| 3:133938490:CACAC:C | acceptor_gain | 1.0000 |
| 3:133938492:CA:C | acceptor_gain | 1.0000 |
| 3:133942764:TAGAT:T | acceptor_gain | 1.0000 |
| 3:133942765:AGAT:A | acceptor_gain | 1.0000 |
| 3:133942766:GAT:G | acceptor_gain | 1.0000 |
| 3:133942769:C:CC | acceptor_gain | 1.0000 |
| 3:133942772:C:CT | acceptor_gain | 1.0000 |
| 3:133942773:A:T | acceptor_gain | 1.0000 |
AlphaMissense
4178 scored. Top likely-pathogenic:
| Variant | Protein change | am_pathogenicity |
|---|---|---|
| 3:133948597:G:C | F348L | 0.999 |
| 3:133948597:G:T | F348L | 0.999 |
| 3:133948599:A:G | F348L | 0.999 |
| 3:133951300:A:G | W257R | 0.998 |
| 3:133951300:A:T | W257R | 0.998 |
| 3:133951297:A:G | W258R | 0.997 |
| 3:133951297:A:T | W258R | 0.997 |
| 3:133951310:C:A | W253C | 0.997 |
| 3:133951310:C:G | W253C | 0.997 |
| 3:133953734:C:T | G218E | 0.997 |
| 3:133973755:C:T | G102D | 0.997 |
| 3:133973793:G:C | S89R | 0.997 |
| 3:133973793:G:T | S89R | 0.997 |
| 3:133973795:T:G | S89R | 0.997 |
| 3:133979526:A:C | F63L | 0.997 |
| 3:133979526:A:T | F63L | 0.997 |
| 3:133979528:A:G | F63L | 0.997 |
| 3:133979530:C:G | R62P | 0.997 |
| 3:133979535:C:A | E60D | 0.997 |
| 3:133979535:C:G | E60D | 0.997 |
| 3:133935839:C:A | W583C | 0.996 |
| 3:133935839:C:G | W583C | 0.996 |
| 3:133953722:C:T | G222E | 0.996 |
| 3:133953735:C:G | G218R | 0.996 |
| 3:133953735:C:T | G218R | 0.996 |
| 3:133955043:C:T | G183E | 0.996 |
| 3:133955050:C:G | G181R | 0.996 |
| 3:133979490:G:C | S75R | 0.996 |
| 3:133979490:G:T | S75R | 0.996 |
| 3:133979492:T:G | S75R | 0.996 |
dbSNP variants (sampled 300 via entrez): RS1000000962 (3:134003481 T>G), RS1000043667 (3:133965163 A>C), RS1000104106 (3:133959916 C>G), RS1000145799 (3:134027586 C>A), RS1000148693 (3:133984310 C>G), RS1000152038 (3:133990933 A>G), RS1000173565 (3:133960052 G>A), RS1000216631 (3:133992857 A>G,T), RS1000221976 (3:133941711 G>A), RS1000277519 (3:134030850 G>A), RS1000283284 (3:133947973 C>T), RS1000368094 (3:133948347 A>T), RS1000432638 (3:134024962 G>C), RS1000468808 (3:133948064 A>G), RS1000520818 (3:133981411 C>T)
Disease associations
OMIM: gene MIM:601460 | disease phenotypes: MIM:167100, MIM:614441, MIM:259100
GenCC curated gene-disease
| Disease | Classification | Inheritance |
|---|---|---|
| hypertrophic osteoarthropathy, primary, autosomal dominant | Definitive | Autosomal dominant |
| hypertrophic osteoarthropathy, primary, autosomal recessive, 2 | Definitive | Autosomal recessive |
| inflammatory bowel disease | Strong | Autosomal recessive |
| pachydermoperiostosis | Supportive | Autosomal recessive |
| chronic enteropathy associated with SLCO2A1 gene | Supportive | Autosomal recessive |
Mondo (6): hypertrophic osteoarthropathy, primary, autosomal dominant (MONDO:0008172), hypertrophic osteoarthropathy, primary, autosomal recessive, 2 (MONDO:0013756), primary hypertrophic osteoarthropathy (MONDO:0016620), (MONDO:0009799), chronic enteropathy associated with SLCO2A1 gene (MONDO:0018766), inflammatory bowel disease (MONDO:0005265)
Orphanet (2): Pachydermoperiostosis (Orphanet:2796), Primary hypertrophic osteoarthropathy (Orphanet:248095)
HPO phenotypes
54 total (30 of 54 shown, HPO-id order):
| HPO | Term |
|---|---|
| HP:0000006 | Autosomal dominant inheritance |
| HP:0000007 | Autosomal recessive inheritance |
| HP:0000280 | Coarse facial features |
| HP:0000508 | Ptosis |
| HP:0000771 | Gynecomastia |
| HP:0000845 | Elevated circulating growth hormone concentration |
| HP:0000939 | Osteoporosis |
| HP:0000964 | Eczematoid dermatitis |
| HP:0000969 | Edema |
| HP:0000975 | Hyperhidrosis |
| HP:0000982 | Palmoplantar keratoderma |
| HP:0001051 | Seborrheic dermatitis |
| HP:0001061 | Acne |
| HP:0001072 | Thickened skin |
| HP:0001217 | Clubbing |
| HP:0001231 | Abnormal fingernail morphology |
| HP:0001369 | Arthritis |
| HP:0001376 | Limitation of joint mobility |
| HP:0001386 | Joint swelling |
| HP:0001744 | Splenomegaly |
| HP:0001903 | Anemia |
| HP:0002024 | Malabsorption |
| HP:0002239 | Gastrointestinal hemorrhage |
| HP:0002240 | Hepatomegaly |
| HP:0002650 | Scoliosis |
| HP:0002653 | Bone pain |
| HP:0002754 | Osteomyelitis |
| HP:0002797 | Osteolysis |
| HP:0002829 | Arthralgia |
| HP:0002970 | Genu varum |
GWAS associations
3 associations (top):
| Study | Trait | p-value |
|---|---|---|
| GCST002337_119 | Amyotrophic lateral sclerosis (sporadic) | 6.000000e-06 |
| GCST007552_34 | Colorectal cancer | 2.000000e-12 |
| GCST008839_554 | Height | 5.000000e-16 |
MeSH disease descriptors (2)
| Descriptor | Name | Tree numbers |
|---|---|---|
| D015212 | Inflammatory Bowel Diseases | C06.405.205.731; C06.405.469.432 |
| D010004 | Osteoarthropathy, Primary Hypertrophic | C05.116.725; C05.550.648; C16.320.718 |
Drugs & pharmacology
Drug and pharmacology data
Is drug target: yes
ChEMBL targets (1): CHEMBL2073703 (SINGLE PROTEIN)
Molecules with ChEMBL bioactivity
1 molecules (phase ≥1), by development phase (incl. off-target/promiscuous compounds). Patent mentions across the top 20 by phase: 3,118 (via chembl_molecule»patent_compound — counts attach to the compound, not the gene–compound relationship, so off-target/promiscuous molecules can dominate).
| Molecule | Name | Phase | Patents |
|---|---|---|---|
| CHEMBL815 | DINOPROST | 4 | 3,118 |
PharmGKB: 1 entry (VIP=true, CPIC=false)
PharmGKB clinical annotations
1 annotations.
| Variant | Type | Level | Drugs | Phenotypes |
|---|---|---|---|---|
| rs34550074 | Toxicity | 3 | Thiazides;plain | Hypertension;Hyponatremia |
PharmGKB variants
1 variants.
| Variant | Genes | Level | Score | #Clin annots | Drugs |
|---|---|---|---|---|---|
| rs34550074 | SLCO2A1 | 3 | 2.50 | 1 | Thiazides;plain |
GtoPdb / IUPHAR curated pharmacology
(IUPHAR/BPS Guide to Pharmacology — expert-curated)
Target class: transporter — SLCO family of organic anion transporting polypeptides
Most potent curated ligand interactions (2 total), top 2:
| Ligand | Action | Affinity | Parameter |
|---|---|---|---|
| bromocresol green | Inhibition | 5.44 | pKi |
| bromsulphthalein | Inhibition | 5.24 | pKi |
Binding affinities (BindingDB)
13 measured of 33 human assays (35 total across all organisms); most potent 13 below. Values come from heterogeneous assays and are not directly comparable.
| Ligand | Measure | Value |
|---|---|---|
| NSC_5311503 | KI | 0.3 nM |
| NSC_3080928 | KI | 0.4 nM |
| CAS_41598-07-6 | KI | 1.7 nM |
| PGI2 | KI | 132 nM |
| AGN 191995 | KI | 228 nM |
| CAS_54751 | KI | 697 nM |
| (Z)-7-[(1R,3R,5S)-3,5-Dihydroxy-2-((E)-(S)-3-hydroxy-oct-1-enyl)-cyclopentyl]-hept-5-enoic acid | KI | 861 nM |
| ILOPROST | KI | 1040 nM |
| CAS_94079-80-8 | KI | 1340 nM |
| CAS_33458-93-4 | KI | 1420 nM |
| PGF2 Alpha, 1-isopropyl ester | KI | 3200 nM |
| U46619 | KI | 3970 nM |
| AGN 191366 | KI | 8130 nM |
ChEMBL bioactivities
3 potent at pChembl≥5 of 3 total, top 3 by pChembl (potency: 10 = 0.1 nM, 6 = 1 µM).
| pChembl | Type | Value | Unit | Molecule |
|---|---|---|---|---|
| 7.64 | Ki | 23 | nM | DINOPROST |
| 7.42 | Ki | 38 | nM | PROSTAGLANDIN D2 |
| 6.83 | Ki | 149 | nM | LATANOPROST ACID |
PubChem BioAssay actives
3 with measured affinity, of 18 total; 3 most potent distinct compounds. Largely complementary to BindingDB; screening values are coarse (µM, 4 dp), so sub-nM hits tie at the floor.
| Compound | Assay | Type | Value | Unit |
|---|---|---|---|---|
| Dinoprost | 679658: TP_TRANSPORTER: inhibition of PGE2 uptake in PGT-expressing HeLa cells | ki | 0.0230 | uM |
| (Z)-7-[(1R,2R,5S)-5-hydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]-3-oxocyclopentyl]hept-5-enoic acid | 679658: TP_TRANSPORTER: inhibition of PGE2 uptake in PGT-expressing HeLa cells | ki | 0.0380 | uM |
| (Z)-7-[(1R,2R,3R,5S)-3,5-dihydroxy-2-[(3R)-3-hydroxy-5-phenylpentyl]cyclopentyl]hept-5-enoic acid | 679659: TP_TRANSPORTER: inhibition of PGE1 uptake (PGE1: 0.0004 uM) in PGT-expressing HeLa cells | ki | 0.1490 | uM |
CTD chemical–gene interactions
64 total (human), top 30 by PubMed support.
| Chemical | Actions (top 5) | PubMed papers |
|---|---|---|
| sodium arsenite | decreases methylation, affects cotreatment, increases abundance, increases expression, decreases expression | 5 |
| Estradiol | increases expression, affects cotreatment, decreases expression, affects binding | 4 |
| bisphenol A | increases expression | 3 |
| Benzo(a)pyrene | affects methylation, increases expression | 3 |
| Aflatoxin B1 | decreases methylation, increases expression, increases methylation | 3 |
| Arsenic | decreases expression, affects cotreatment, increases abundance | 2 |
| Diethylhexyl Phthalate | increases expression, affects cotreatment, affects reaction | 2 |
| Progesterone | increases reaction, affects cotreatment, decreases expression, affects expression | 2 |
| Tobacco Smoke Pollution | decreases expression | 2 |
| Genistein | increases expression | 2 |
| aristolochic acid I | decreases expression | 1 |
| bisphenol F | increases expression | 1 |
| Esketamine | decreases expression | 1 |
| bufotalin | decreases expression | 1 |
| diethyl phthalate | increases expression, affects cotreatment, affects reaction | 1 |
| lead acetate | decreases expression | 1 |
| diisononyl phthalate | increases expression, affects cotreatment, affects reaction | 1 |
| ethyl-p-hydroxybenzoate | increases expression | 1 |
| o,p’-DDT | increases expression | 1 |
| sulforaphane | decreases expression | 1 |
| perfluorooctanoic acid | increases expression | 1 |
| tobacco tar | decreases expression | 1 |
| manganese chloride | affects cotreatment, decreases expression, increases abundance | 1 |
| diisobutyl phthalate | increases expression, affects cotreatment, affects reaction | 1 |
| butylbenzyl phthalate | affects cotreatment, affects reaction, increases expression | 1 |
| cupric chloride | decreases expression | 1 |
| perfluorooctane sulfonic acid | increases expression | 1 |
| perfluoro-n-nonanoic acid | increases expression | 1 |
| lumiracoxib | decreases reaction, increases transport | 1 |
| bisphenol S | increases expression | 1 |
ChEMBL screening assays
4 unique, capped per target: 4 functional
Representative assays (with source publication via chembl_document):
| Assay ID | Type | Description | Source paper |
|---|---|---|---|
| CHEMBL2075322 | Functional | TP_TRANSPORTER: inhibition of PGE2 uptake in PGT-expressing HeLa cells | Cloning of mouse prostaglandin transporter PGT cDNA: species-specific substrate affinities. — Am J Physiol |
Cellosaurus cell lines
2 cell lines: 2 cancer cell line
First 10 cell lines (id-ordered, not curated):
| Cellosaurus | Name | Category | Sex |
|---|---|---|---|
| CVCL_D4UQ | HuH7-SLCO2A1-KO-c2 | Cancer cell line | Male |
| CVCL_D4UR | HuH7-SLCO2A1-KO-c3 | Cancer cell line | Male |
Clinical trials (associated diseases)
301 trials via MONDO — disease-level, not drug-specific.
| Trial | Phase | Status | Title |
|---|---|---|---|
| NCT00167882 | PHASE4 | COMPLETED | The Influence of 5-Aminosalicylates on Thiopurine Metabolite Levels |
| NCT00205062 | PHASE4 | TERMINATED | Positron Emission Tomography (PET)-Computed Tomography (CT) in Inflammatory Bowel Disease (IBD) |
| NCT00567593 | PHASE4 | COMPLETED | Gene Regulation by Thiazolidinediones |
| NCT00746395 | PHASE4 | COMPLETED | Randomized, Placebo-controlled Trial of Lubiprostone as a Preparation for Capsule Endoscopy |
| NCT01034358 | PHASE4 | COMPLETED | Immune Response to the Human Papillomavirus Vaccine in Young Women With Inflammatory Bowel Disease |
| NCT01056913 | PHASE4 | COMPLETED | NITI CAR27 (ColonRing) Compression Anastomosis in Colorectal Surgery |
| NCT01067547 | PHASE4 | COMPLETED | A Trial of Iron Replacement in Patients With Iron Deficiency. |
| NCT01341808 | PHASE4 | COMPLETED | Immunogenicity of Hepatitis A Vaccine in Inflammatory Bowel Disease (IBD) Patients |
| NCT01908283 | PHASE4 | COMPLETED | Induction of Immunity Against Streptococcus Pneumoniae in Adults With Inflammatory Bowel Disease |
| NCT01934088 | PHASE4 | COMPLETED | Satisfaction With Nurse Administered Propofol Sedation vs. Midazolam With Fentanyl Sedation for Endoscopy |
| NCT02162862 | PHASE4 | COMPLETED | Treating Disrupted Sleep in Individuals With Inflammatory Bowel Disease |
| NCT02248337 | PHASE4 | COMPLETED | Low Volume Colon Preparation for IBD |
| NCT02281799 | PHASE4 | WITHDRAWN | Thiopurine Induced Pancreatitis in IBD Patients |
| NCT02392286 | PHASE4 | TERMINATED | Corticosteroid Dosage for Crohn’s Disease Flare |
| NCT02437591 | PHASE4 | COMPLETED | Study to Evaluate the Pharmacokinetics of Fidaxomicin in Inflammatory Bowel Disease (IBD) Subjects With Clostridium Difficile Infection (CDI) |
| NCT02453776 | PHASE4 | COMPLETED | Precision Dosing of Infliximab Versus Conventional Dosing of Infliximab |
| NCT02461758 | PHASE4 | COMPLETED | Trial of High Dose vs. Standard Dose Influenza Vaccine in Inflammatory Bowel Disease Patients |
| NCT02566889 | PHASE4 | TERMINATED | An Efficacy and Safety Study of Infliximab Dose Escalation in Pediatric Participants With Inflammatory Bowel Disease |
| NCT02774057 | PHASE4 | UNKNOWN | Trial of Captafer® vs. Oral Iron Sulfate in the Treatment of Iron Deficiency Anemia in Patients With IBD |
| NCT02806206 | PHASE4 | UNKNOWN | Prucalopride Prior to Small Bowel Capsule Endoscopy |
| NCT02946203 | PHASE4 | COMPLETED | Comparison of VoLumen and Breeza Oral Contrast Agents in Pediatric Patients |
| NCT02994836 | PHASE4 | COMPLETED | GIS-SUSANTI-TNF-2015 (Anti-TNF Discontinuation ) |
| NCT03220841 | PHASE4 | UNKNOWN | Stricture Definition and Treatment (STRIDENT) Drug Therapy Study |
| NCT03351972 | PHASE4 | COMPLETED | Differences in Preparation for Small Bowel Capsule Endoscopy |
| NCT03466983 | PHASE4 | COMPLETED | A Trial Comparing the Incidence of Hypophosphatemia in Relation to Treatment With Iron Isomaltoside and Ferric Carboxymaltose in Subjects With Iron Deficiency Anaemia Due to Inflammatory Bowel Disease |
| NCT03591770 | PHASE4 | TERMINATED | Shingrix Vaccine in Patients With Moderate to Severe Ulcerative Colitis on Tofacitinib |
| NCT03629379 | PHASE4 | COMPLETED | Response to Ustekinumab for Anti-tnf Induced Psoriasiform Skin Lesions |
| NCT03723447 | PHASE4 | COMPLETED | Intraoperative TAP Block With Bupivacaine/Dexamethasone Against Liposomal Bupivacaine (Exparel®) |
| NCT03798691 | PHASE4 | COMPLETED | Immunogenicity of Herpes Zoster Subunit Vaccine in Inflammatory Bowel Disease Patients Treated With Vedolizumab |
| NCT03860012 | PHASE4 | UNKNOWN | Folic Acid in Pediatric Inflammatory Bowel Disease |
| NCT03885713 | PHASE4 | COMPLETED | Identification of Predictive Biomarkers for Response to Biologic Therapies and Tofacitinib in Inflammatory Bowel Disease |
| NCT03917303 | PHASE4 | RECRUITING | Control Crohn Safe Trial |
| NCT04045782 | PHASE4 | COMPLETED | Evaluation of the Safety and Effectiveness of Switching From Humira® to Imraldi® in Flanders |
| NCT04304950 | PHASE4 | COMPLETED | Chronotherapy in Inflammatory Bowel Disease |
| NCT04626947 | PHASE4 | TERMINATED | Prevention of Recurrent Clostridium Difficile Infection (CDI) in Patients With Inflammatory Bowel Disease (IBD). |
| NCT04646187 | PHASE4 | ENROLLING_BY_INVITATION | De-escalation of Anti-TNF Therapy in Inflammatory Bowel Disease |
| NCT04835506 | PHASE4 | ACTIVE_NOT_RECRUITING | Proactive Infliximab Optimization Using a Pharmacokinetic Dashboard Versus Standard of Care in Patients With Inflammatory Bowel Disease: The OPTIMIZE Trial |
| NCT04982172 | PHASE4 | COMPLETED | Model-informed Dose De-escalation of Infliximab in Patients With Inflammatory Bowel Diseases |
| NCT05180175 | PHASE4 | COMPLETED | The Nordic IBD Treatment Strategy Trial |
| NCT05280405 | PHASE4 | UNKNOWN | Early Proactive Therapeutic Drug Monitoring of Infliximab in Children: EPIC Study |
Related Atlas pages
- Associated diseases: hypertrophic osteoarthropathy, primary, autosomal dominant, hypertrophic osteoarthropathy, primary, autosomal recessive, 2, primary hypertrophic osteoarthropathy, chronic enteropathy associated with SLCO2A1 gene, inflammatory bowel disease
- Disease cohort memberships (association, not causation — diseases whose associated-gene cohort lists this gene; a subset are also under Associated diseases): chronic enteropathy associated with SLCO2A1 gene, hypertrophic osteoarthropathy, primary, autosomal dominant, hypertrophic osteoarthropathy, primary, autosomal recessive, 2, inflammatory bowel disease, primary hypertrophic osteoarthropathy, sporadic amyotrophic lateral sclerosis