Chemical Research Center, Institute of Biomolecular Chemistry, HAS, Budapest, Hungary.
Drug Metab Rev. 2010 Aug;42(3):402-36. doi: 10.3109/03602530903491741.
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.
ABCC2/Abcc2（MRP2/Mrp2）表达于主要的生理屏障，如肝细胞的胆小管膜、肾近端小管上皮细胞、小肠和大肠的肠上皮细胞以及胎盘的合体滋养层。ABCC2/Abcc2 始终定位于顶膜。尽管 ABCC2/Abcc2 转运多种属于不同分子类别的两亲性阴离子，如内源性化合物（如胆红素-葡糖苷酸）、药物、有毒化学品、营养保健品及其缀合物，但它对 II 相缀合物具有偏好性。表型上，导致 Dubin-Johnson 综合征的 ABCC2 突变最明显的后果是结合胆红素血症。ABCC2/Abcc2 含有多个结合位点，并表现出复杂的转运动力学。
