SLCO1B1 Antibody – Mouse Monoclonal

This gene encodes a liver-specific member of the organic anion transporter family. The encoded protein is a transmembrane receptor that mediates the sodium-independent uptake of numerous endogenous compounds including bilirubin, 17-beta-glucuronosyl estradiol and leukotriene C4. This protein is also involved in the removal of drug compounds such as statins, bromosulfophthalein and rifampin from the blood into the hepatocytes. Polymorphisms in the gene encoding this protein are associated with impaired transporter function. [provided by RefSeq]

SLCO1B1: Mediates the Na(+)-independent uptake of organic anions such as pravastatin, taurocholate, methotrexate, dehydroepiandrosterone sulfate, 17-beta-glucuronosyl estradiol, estrone sulfate, prostaglandin E2, thromboxane B2, leukotriene C3, leukotriene E4, thyroxine and triiodothyronine. Involved in the clearance of bile acids and organic anions from the liver. Defects in SLCO1B1 are a cause of hyperbilirubinemia, Rotor type (HBLRR). An autosomal recessive form of primary conjugated hyperbilirubinemia. Affected individuals develop mild jaundice not associated with hemolysis shortly after birth or in childhood. They have delayed plasma clearance of the unconjugated anionic dye bromsulphthalein and prominent urinary excretion of coproporphyrin I. Hepatic pigmentation is normal. Belongs to the organo anion transporter (TC 2.A.60) family.

Protein type: Transporter; Transporter, SLC family; Membrane protein, multi-pass; Membrane protein, integral

Chromosomal Location of Human Ortholog: 12p

Cellular Component: membrane; basolateral plasma membrane; integral to plasma membrane; plasma membrane

Molecular Function: sodium-independent organic anion transmembrane transporter activity

Biological Process: bile acid and bile salt transport; sodium-independent organic anion transport; bile acid metabolic process; transmembrane transport; organic anion transport

Disease: Hyperbilirubinemia, Rotor Type