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金黄色葡萄球菌 HPPK 的结构和新型底物结合位点抑制剂的发现。

Structure of S. aureus HPPK and the discovery of a new substrate site inhibitor.

机构信息

Medicinal Chemistry and Drug Action, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Australia.

出版信息

PLoS One. 2012;7(1):e29444. doi: 10.1371/journal.pone.0029444. Epub 2012 Jan 19.

Abstract

The first structural and biophysical data on the folate biosynthesis pathway enzyme and drug target, 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase (SaHPPK), from the pathogen Staphylococcus aureus is presented. HPPK is the second essential enzyme in the pathway catalysing the pyrophosphoryl transfer from cofactor (ATP) to the substrate (6-hydroxymethyl-7,8-dihydropterin, HMDP). In-silico screening identified 8-mercaptoguanine which was shown to bind with an equilibrium dissociation constant, K(d), of ∼13 µM as measured by isothermal titration calorimetry (ITC) and surface plasmon resonance (SPR). An IC(50) of ∼41 µM was determined by means of a luminescent kinase assay. In contrast to the biological substrate, the inhibitor has no requirement for magnesium or the ATP cofactor for competitive binding to the substrate site. The 1.65 Å resolution crystal structure of the inhibited complex showed that it binds in the pterin site and shares many of the key intermolecular interactions of the substrate. Chemical shift and (15)N heteronuclear NMR measurements reveal that the fast motion of the pterin-binding loop (L2) is partially dampened in the SaHPPK/HMDP/α,β-methylene adenosine 5'-triphosphate (AMPCPP) ternary complex, but the ATP loop (L3) remains mobile on the µs-ms timescale. In contrast, for the SaHPPK/8-mercaptoguanine/AMPCPP ternary complex, the loop L2 becomes rigid on the fast timescale and the L3 loop also becomes more ordered--an observation that correlates with the large entropic penalty associated with inhibitor binding as revealed by ITC. NMR data, including (15)N-(1)H residual dipolar coupling measurements, indicate that the sulfur atom in the inhibitor is important for stabilizing and restricting important motions of the L2 and L3 catalytic loops in the inhibited ternary complex. This work describes a comprehensive analysis of a new HPPK inhibitor, and may provide a foundation for the development of novel antimicrobials targeting the folate biosynthetic pathway.

摘要

本文首次报道了病原体金黄色葡萄球菌中叶酸生物合成途径酶和药物靶点 6-羟甲基-7,8-二氢蝶呤焦磷酸激酶(SaHPPK)的结构和生物物理数据。HPPK 是该途径中的第二个必需酶,催化辅酶(ATP)与底物(6-羟甲基-7,8-二氢蝶呤,HMDP)之间的焦磷酸基转移。基于计算机的筛选鉴定出 8-巯基鸟嘌呤,其通过等温滴定量热法(ITC)和表面等离子体共振(SPR)测定的平衡解离常数 K(d)约为 13µM。通过发光激酶测定确定的 IC(50)约为 41µM。与生物底物不同,该抑制剂在与底物结合部位竞争结合时不需要镁或 ATP 辅酶。抑制复合物的 1.65Å分辨率晶体结构表明,它结合在蝶呤部位,并与底物的许多关键分子间相互作用共享。化学位移和 (15)N 异核 NMR 测量表明,在 SaHPPK/HMDP/α,β-亚甲基腺苷 5'-三磷酸(AMPCPP)三元复合物中,蝶呤结合环(L2)的快速运动部分被抑制,但 ATP 环(L3)在 µs-ms 时间尺度上仍然是移动的。相比之下,对于 SaHPPK/8-巯基鸟嘌呤/AMPCPP 三元复合物,L2 环在快速时间尺度上变得刚性,L3 环也变得更加有序——这一观察结果与 ITC 揭示的与抑制剂结合相关的大熵罚相关。NMR 数据,包括 (15)N-(1)H 残差偶极耦合测量,表明抑制剂中的硫原子对于稳定和限制抑制三元复合物中 L2 和 L3 催化环的重要运动非常重要。这项工作描述了对新型 HPPK 抑制剂的全面分析,可能为针对叶酸生物合成途径开发新型抗菌药物提供基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8dbf/3261883/f0799009be45/pone.0029444.g001.jpg

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