Journal
DRUG METABOLISM REVIEWS
Volume 42, Issue 3, Pages 402-436Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/03602530903491741
Keywords
ABCC2; MRP2; ABC transporter; Dubin-Johnson syndrome; conjugate hyperbilirubinemia; pharmacokinetics; ADME; toxicity
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Funding
- Hungarian grant [XTTPSRT1]
- European Community [Lintop-LSHB-CT-2006-037499, Memtrans-LSHBCT-2006-518246]
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ABCC2/Abcc2 (MRP2/Mrp2) is expressed at major physiological barriers, such as the canalicular membrane of liver cells, kidney proximal tubule epithelial cells, enterocytes of the small and large intestine, and syncytiotrophoblast of the placenta. ABCC2/Abcc2 always localizes in the apical membranes. Although ABCC2/Abcc2 transports a variety of amphiphilic anions that belong to different classes of molecules, such as endogenous compounds (e. g., bilirubin-glucuronides), drugs, toxic chemicals, nutraceuticals, and their conjugates, it displays a preference for phase II conjugates. Phenotypically, the most obvious consequence of mutations in ABCC2 that lead to Dubin-Johnson syndrome is conjugate hyperbilirubinemia. ABCC2/Abcc2 harbors multiple binding sites and displays complex transport kinetics.
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