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The Interaction of ApoA-I and ABCA1 Triggers Signal Transduction Pathways to Mediate Efflux of Cellular Lipids

机译:ApoA-I和ABCA1的相互作用触发信号转导途径介导细胞脂质的外流。

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摘要

Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATP-binding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1. ApoA-I increases the levels of ABCA1 protein markedly. In turn, ABCA1 can stabilize apoA-I. The interaction of apoA-I with ABCA1 could activate signaling molecules that modulate posttranslational ABCA1 activity or lipid transport activity. The key signaling molecules in these processes include protein kinase A (PKA), protein kinase C (PKC), Janus kinase 2 (JAK2), Rho GTPases and Ca2+, and many factors also could influence the interaction of apoA-I with ABCA1. This review will summarize these mechanisms for the apoA-I interaction with ABCA1 as well as the signal transduction pathways involved in these processes.
机译:胆固醇逆向转运(RCT)已被描述为抗动脉粥样硬化的关键步骤,这是由ATP结合盒A1(ABCA1)启动,以介导细胞磷脂和胆固醇向无脂质载脂蛋白A-I(apoA-I)的流出。然而,对apoA-I / ABCA1相互作用导致apoA-I脂质化的潜在机制了解甚少。针对apoA-I与ABCA1的相互作用以及ABCA1介导的apoA-I的脂化,提出了几种模型。 ApoA-I显着增加ABCA1蛋白的水平。反过来,ABCA1可以稳定apoA-I。 apoA-I与ABCA1的相互作用可以激活调节翻译后ABCA1活性或脂质转运活性的信号分子。这些过程中的关键信号传导分子包括蛋白激酶A(PKA),蛋白激酶C(PKC),Janus激酶2(JAK2),Rho GTPases和Ca 2 + ,许多因素也可能影响蛋白质的表达。 apoA-I与ABCA1的相互作用。这篇综述将总结这些apoA-I与ABCA1相互作用的机制以及这些过程中涉及的信号转导途径。

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