SLCO2A1, the official full name is solute carrier organic anion transporter family member 2A1, which owns 12 transmembrane domains. It is encoded by the SLCO2A1 gene in humans and belongs to SLC21A family of solute carriers. This gene is conserved in chimpanzee, cow, chicken, rat, dog, mouse, Rhesus monkey, and frog. 227 organisms have orthologs with this gene. SLCO2A1 is broadly expressed in lung, thyroid, and 20 other tissues, and is involved in uptake and clearance of prostaglandins in different tissues.
|Basic Information of SLCO2A1|
|Protein Name||Solute carrier organic anion transporter family member 2A1|
|Organism||Homo sapiens (Human)|
SLCO2A1 is also known as solute carrier family 21 member 2 (SLC21A2), which belongs to the 12-membrane-spanning superfamily of solute carriers. As a member of the prostaglandin transporter and organic anion transporter family, SLCO2A1 mediates uptake and clearance of prostaglandins in different tissues. Also, SLCO2A1 is a necessary core component of the Maxi-Cl channel which is the most efficient pathway to regulate the fluxes of inorganic and organic anions including ATP. In addition, SLCO2A1 is highly associated with colon cancer progression through PGE2 uptake into the endothelial cells. Moreover, it plays a functional role in the metabolic clearance of prostaglandins. These reported functions are located at cytoplasmic vesicle or organelle membranes. It’s associated with various physiological and pathophysiological processes in diverse organs. Furthermore, mutations in SLCO2A1 are associated with primary hypertrophic osteoarthropathy, and SLCO2A1 is necessary for body temperature modulation during fever.
Fig.1 Crystal structure of wild-type SLCO2A1. (Cheng, 2013)
This article indicates that the SLCO2A1 is a necessary core component of the Maxi-Cl channel.
This article demonstrates that SLCO2A1 can promote tumor progression through PGE2 uptake into the endothelial cells, and SLCO2A1 inhibition can improve colon cancer outcomes.
This article shows the physiological and pathological importance mediated by SLCO2A1.
This article shows that the primary hypertrophic osteoarthropathy with mutated SLCO2A1 can be treated with Etoricoxib in a Chinese patient.
This article shows the new genetic variants of SLCO2A1 in Mexican patients with primary hypertrophic osteoarthropathy.
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