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SLCO2A1 encodes a prostaglandin transporter that is a member of the 12-membrane-spanning superfamily of transporters. Additionally we are shipping SLCO2A1 Antibodies (27) and many more products for this protein.
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Because no phenotype associated differences could be found in the gene sequence nor in its jejunal transcription profile, SLCO2A1 can most likely be excluded as receptor for F4 bacteria.
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.
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
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.
A novel missense mutation c.101T > C in the SLCO2A1 gene causes pachydermoperiostosis of the complete type.
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.
We herein report patients with pachydermoperiostosis (PDP (show PDP Proteins))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 (show PDP Proteins) in the Korean population.
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).
In this article we describe a novel mutation in the SLCO2A1 causing Pachydermoperiostosis in a Lebanese family
overexpression of SLCO2A1 could induce and knockdown inhibit the invasion of lung cancer cells. expression levels of p-mTOR (show FRAP1 Proteins), p-AKT (show AKT1 Proteins) and p-S6 were up-regulated or down-regulated with the overexpression or knockdown of SLCO2A1.
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
SLCO2A1 is an essential core component of the ATP-conductive Maxi-Cl channel.
Data suggest that prostaglandin E3 (PGE3) metabolism is downregulated in prostaglandin transporter Slco2a1(-/-) knockout mice.
Slco2a1 contributes to PGE2 secretion by macrophages via exocytosis.
Pulmonary Prostaglandin E2 disposition is largely regulated by SLCO2A1, demonstrating that SLCO2A1 plays a critical role in protecting the lung from Bleomycin-induced fibrosis.
Prostaglandin transporter plays a critical role in closure of the ductus arteriosus after birth by ensuring a reduction in local and/or circulating PGE (show LIPF Proteins)(2) concentrations.
Renal collecting duct prostaglandin transporter transcription varied with dietary salt intake.
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.
solute carrier organic anion transporter family, member 2A1
, matrin F/G 1
, prostaglandin transporter
, solute carrier family 21 (prostaglandin transporter), member 2
, solute carrier family 21 member 2
, solute carrier organic anion transporter family member 2A1