SLCO1B3

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SLCO1B3

A gene on chromosome 12p12 that encodes a transporter which mediates Na+-independent uptake of organic anions—e.g., oestradiol, taurocholate, triiodothyronine, leukotriene C4, dehydroepiandrosterone sulfate, methotrexate and sulfobromophthalein.
 
Molecular pathology
Defects in SLCO1B3 are a cause of Rotor syndrome.
References in periodicals archive ?
Molecular mechanisms governing different pharmacokinetics of ginsenosides and potential for ginsenoside-perpetrated herb-drug interactions on OATP1B3.
The transporters recommended for initial assessment generally Included those for which A clinical relevance to drug disposition has Been identified, namely, the efflux transporters P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), and the uptake transporters OCT2, OAT1, OAT3, OATP1B1 and OATP1B3.
Expression of OATP1B3 determines uptake of Gd-EOB-DTPA in hepatocellular carcinoma.
Role of the liver-specific transporters OATP1B1 and OATP1B3 in governing drug elimination.
Because of the structure and size of MCs, active uptake into cells occurs via organic anion-transporting polypeptides (OATP/Oatp), as confirmed for liver-specific human OATP1B1 and OATP1B3, mouse Oatp1b2 (mOatp 1b2), skate Oatp 1d1, and the more widely distributed OATP1A2 expressed, for example, at the blood--brain barrier.
Involvement of mitogen-activated protein kinase signaling pathways in microcystin-LR-induced apoptosis after its selective uptake mediated by OATP1B1 and OATP1B3.
Transport of fluorescent chenodeoxycholic acid via the human organic anion transporters OATP1B1 and OATP1B3.
The seven identified transporters are: the efflux transporters P-glycoprotein (P-gp, MDR1, ABCB1) and BCRP (ABCG2); organic cation transporter OCT2 (SLC22A2); organic anion transporters OAT1 (SLC22A6) and OAT3 (SLC22A8); and organic anion-transporting polypeptides OATP1B1 (SLCO1B1) and OATP1B3 (SLCO1B3).
KEY WORDS: Akt, apoptosis, [beta]-catenin, cyclin D1, GSK-3[beta], microcystin-LR, OATP1B3, p53, proliferation, siah-1.
2007) reported that the expression of the human hepatocyte uptake transporter OATP1B1 or OATP1B3 was critical for the selective uptake of microcystin-LR into hepatocytes and for induction of its fatal cytotoxicity.
In the present study, we used wild-type p53-expressing HEK293 human embryonic kidney cells stably transfected with OATP1B3, to demonstrate that a lethal concentration of microcystin-LR stimulated not only cellular signal transduction, leading to cell death, but also cell survival signals.
These agents may fall into the category of inhibitory or competitive OATP1B3 substrates, which may inhibit uptake of the toxin.