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首页> 外文期刊>Current opinion in lipidology >ATP-binding cassette transporter AI and its role in HDL formation.
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ATP-binding cassette transporter AI and its role in HDL formation.

机译：ATP结合盒转运蛋白AI及其在HDL形成中的作用。

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PURPOSE OF REVIEW: ATP-binding cassette transporter AI (ABCA1)-mediated assembly of phospholipid and free cholesterol with apoA-I plays an important role in HDL biogenesis. This review focuses on recent progress in ABCA1-mediated HDL formation and regulation of ABCA1 expression. RECENT FINDINGS: Studies of hepatic ABCA1 overexpression suggest that the liver is a major site for HDL formation. Lipidation of apoA-I by ABCA1 increases its potential for reverse cholesterol transport based on the following findings: (1) apoA-I/lipid complexes formed by ABCA1 are better acceptors of cellular lipid via non-ABCA1-mediated efflux pathways than lipid-free apoA-I in vitro and (2) lipidation of apoA-I prevents it from rapidly associating with plasma HDL in vivo, resulting in more available nascent pre-beta HDL for cellular lipid efflux. Several novel regulatory mechanisms for ABCA1 at the post-transcriptional level have been identified recently. Interaction of apoA-I with ABCA1 prevents phosphorylation of a sequence rich in proline, glutamic acid, serine and threonine in a cytoplasmic domain of ABCA1, resulting in less degradation by calpain proteolysis and increased surface expression of ABCA1. In addition, destabilization and decreased cellular surface expression of ABCA1 protein by unsaturated fatty acids have been identified. SUMMARY: Initial lipidation of apoA-I by hepatic ABCA1 is critical for plasma HDL formation because it enables pre-beta HDL to function more efficiently as a cholesterol acceptor for other pathways of cholesterol efflux in the reverse cholesterol transport pathway and prevents apoA-I from rapidly associating with preexisting plasma HDL particles, resulting in greater availability of pre-beta HDL particles for cholesterol efflux.
机译：审查目的：ATP结合盒转运蛋白AI（ABCA1）介导的磷脂和游离胆固醇与apoA-I的组装在HDL生物发生中起重要作用。这篇综述着重于ABCA1介导的HDL形成和ABCA1表达调控的最新进展。最近的发现：肝ABCA1过表达的研究表明，肝脏是HDL形成的主要部位。基于以下发现，ABCA1对apoA-I的脂化作用增加了其逆向胆固醇转运的潜力：（1）由ABCA1形成的apoA-I /脂质复合物比非脂质通过非ABCA1介导的外排途径更好地接受细胞脂质体外载脂蛋白A-1和（2）载脂蛋白A-I的脂质化阻止它与体内血浆HDL快速关联，从而导致更多可用的新生β-前HDL用于细胞脂质外排。最近已经确定了转录后水平上ABCA1的几种新型调节机制。 apoA-I与ABCA1的相互作用可防止ABCA1胞质域中富含脯氨酸，谷氨酸，丝氨酸和苏氨酸的序列的磷酸化，从而减少钙蛋白酶蛋白酶解的降解并增加ABCA1的表面表达。此外，已经发现不饱和脂肪酸会破坏ABCA1蛋白的稳定性并降低其细胞表面表达。简介：肝ABCA1对apoA-I的初始脂化对于血浆HDL形成至关重要，因为它使前beta HDL能够更有效地用作胆固醇在逆向胆固醇转运途径中的其他途径的胆固醇受体，并阻止apoA-I的发生。快速地与先前存在的血浆HDL颗粒缔合，从而提高了beta-HDL颗粒用于胆固醇外流的可用性。

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