Department of Chemistry and Biochemistry, University of California at San Diego , La Jolla, California 92093, United States.
Biochemistry. 2013 Aug 6;52(31):5295-303. doi: 10.1021/bi4006623. Epub 2013 Jul 24.
Hepatitis C virus (HCV) protein p7 plays an important role in the assembly and release of mature virus particles. This small 63-residue membrane protein has been shown to induce channel activity, which may contribute to its functions. p7 is highly conserved throughout the entire range of HCV genotypes, which contributes to making p7 a potential target for antiviral drugs. The secondary structure of p7 from the J4 genotype and the tilt angles of the helices within bilayers have been previously characterized by nuclear magnetic resonance (NMR). Here we describe the three-dimensional structure of p7 in short chain phospholipid (1,2-dihexanoyl-sn-glycero-3-phosphocholine) micelles, which provide a reasonably effective membrane-mimicking environment that is compatible with solution NMR experiments. Using a combination of chemical shifts, residual dipolar couplings, and PREs, we determined the structure of p7 using an implicit membrane potential combining both CS-Rosetta decoys and Xplor-NIH refinement. The final set of structures has a backbone root-mean-square deviation of 2.18 Å. Molecular dynamics simulations in NAMD indicate that several side chain interactions might be taking place and that these could affect the dynamics of the protein. In addition to probing the dynamics of p7, we evaluated several drug-protein and protein-protein interactions. Established channel-blocking compounds such as amantadine, hexamethylene amiloride, and long alkyl chain iminosugar derivatives inhibit the ion channel activity of p7. It has also been shown that the protein interacts with HCV nonstructural protein 2 at the endoplasmic reticulum and that this interaction may be important for the infectivity of the virus. Changes in the chemical shift frequencies of solution NMR spectra identify the residues taking part in these interactions.
丙型肝炎病毒 (HCV) 蛋白 p7 在成熟病毒颗粒的组装和释放中发挥重要作用。这种 63 个残基的小膜蛋白已被证明具有诱导通道活性的作用,这可能与其功能有关。p7 在整个 HCV 基因型范围内高度保守,这有助于使其成为抗病毒药物的潜在靶标。J4 基因型的 p7 的二级结构和双层内螺旋的倾斜角度已通过核磁共振 (NMR) 进行了先前的表征。在这里,我们描述了 p7 在短链磷脂(1,2-二己酰基-sn-甘油-3-磷酸胆碱)胶束中的三维结构,该结构提供了一种合理有效的膜模拟环境,与溶液 NMR 实验兼容。我们使用化学位移、残差偶极耦合和 PREs 的组合,使用结合了 CS-Rosetta 诱饵和 Xplor-NIH 细化的隐含膜电势来确定 p7 的结构。最终结构集的骨架均方根偏差为 2.18 Å。NAMD 的分子动力学模拟表明,可能存在几种侧链相互作用,并且这些相互作用可能会影响蛋白质的动力学。除了探测 p7 的动力学外,我们还评估了几种药物-蛋白质和蛋白质-蛋白质相互作用。已建立的通道阻断化合物,如金刚烷胺、六亚甲基阿米洛利和长烷基链亚氨基糖衍生物,抑制 p7 的离子通道活性。还表明该蛋白与内质网中的 HCV 非结构蛋白 2 相互作用,这种相互作用对于病毒的感染力可能很重要。溶液 NMR 光谱的化学位移频率变化可识别参与这些相互作用的残基。