Regulation of hepatic ABCC transporters by xenobiotics and in disease states.
Regulation of hepatic ABCC transporters by xenobiotics and in disease states.
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DOI：
10.3109/03602531003654915
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发表时间：
2010-08
影响因子：
5.9
通讯作者：
Manautou JE
中科院分区：
文献类型：
--
作者：
Gu X;Manautou JE
ABCC转运蛋白家族由哺乳动物中的13个成员组成，包括多药耐药相关蛋白(MRPs)、磺脲类受体(SURS)和囊性纤维化跨膜传导调节因子(CFTR)。这些蛋白质在化学解毒、处置和正常细胞生理中发挥作用。ABCC转运蛋白在肝脏中差异表达，并在转录和翻译水平上受到调控。它们的表达和功能也受翻译后修饰和膜转运事件的控制。这些过程受到严格监管。有关肝胆ABCC转运蛋白表达变化的信息可以为疾病的发病机制和外源物质的处置提供重要的见解。在这篇综述中，我们描述了在疾病状态下以及在缺乏转录因子、转运蛋白和细胞信号分子的转基因动物模型中，各种外源生物对人类和啮齿动物肝脏ABCC转运蛋白的调节。
The subfamily of ABCC transporters consists of 13 members in mammals, including the multidrug resistance-associated proteins (MRPs), sulfonylurea receptors (SURs), and the cystic fibrosis transmembrane conductance regulator (CFTR). These proteins play roles in chemical detoxification, disposition, and normal cell physiology. ABCC transporters are expressed differentially in the liver and are regulated at the transcription and translation level. Their expression and function are also controlled by post-translational modification and membrane-trafficking events. These processes are tightly regulated. Information about alterations in the expression of hepatobiliary ABCC transporters could provide important insights into the pathogenesis of diseases and disposition of xenobiotics. In this review, we describe the regulation of hepatic ABCC transporters in humans and rodents by a variety of xenobiotics, under disease states and in genetically modified animal models deficient in transcription factors, transporters, and cell-signaling molecules.
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