Ajees A Abdul, Anantharamaiah G M, Mishra Vinod K, Hussain M Mahmood, Murthy H M Krishna
Center for Biophysical Sciences and Engineering and Atherosclerosis Research Unit and Department of Medicine, University of Alabama, 1530 3rd Avenue South, Birmingham, AL 35294, USA.
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2126-31. doi: 10.1073/pnas.0506877103. Epub 2006 Feb 1.
Despite three decades of extensive studies on human apolipoprotein A-I (apoA-I), the major protein component in high-density lipoproteins, the molecular basis for its antiatherogenic function is elusive, in part because of lack of a structure of the full-length protein. We describe here the crystal structure of lipid-free apoA-I at 2.4 A. The structure shows that apoA-I is comprised of an N-terminal four-helix bundle and two C-terminal helices. The N-terminal domain plays a prominent role in maintaining its lipid-free conformation, indicating that mutants with truncations in this region form inadequate models for explaining functional properties of apoA-I. A model for transformation of the lipid-free conformation to the high-density lipoprotein-bound form follows from an analysis of solvent-accessible hydrophobic patches on the surface of the structure and their proximity to the hydrophobic core of the four-helix bundle. The crystal structure of human apoA-I displays a hitherto-unobserved array of positively and negatively charged areas on the surface. Positioning of the charged surface patches relative to hydrophobic regions near the C terminus of the protein offers insights into its interaction with cell-surface components of the reverse cholesterol transport pathway and antiatherogenic properties of this protein. This structure provides a much-needed structural template for exploration of molecular mechanisms by which human apoA-I ameliorates atherosclerosis and inflammatory diseases.
尽管对人类载脂蛋白A-I(apoA-I)进行了三十年的广泛研究,它是高密度脂蛋白中的主要蛋白质成分,但其抗动脉粥样硬化功能的分子基础仍不清楚,部分原因是缺乏全长蛋白质的结构。我们在此描述了无脂质apoA-I在2.4埃分辨率下的晶体结构。该结构表明,apoA-I由一个N端四螺旋束和两个C端螺旋组成。N端结构域在维持其无脂质构象方面起着重要作用,这表明该区域有截短的突变体不能很好地解释apoA-I的功能特性。通过分析该结构表面可溶剂接触的疏水区域及其与四螺旋束疏水核心的接近程度,得出了从无脂质构象转变为高密度脂蛋白结合形式的模型。人类apoA-I的晶体结构在表面展示了一系列迄今未被观察到的带正电和带负电的区域。带电荷的表面区域相对于蛋白质C端附近疏水区域的定位,为深入了解其与逆向胆固醇转运途径的细胞表面成分的相互作用以及该蛋白质的抗动脉粥样硬化特性提供了线索。该结构为探索人类apoA-I改善动脉粥样硬化和炎症性疾病的分子机制提供了急需的结构模板。