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人源 MDR1 P-糖蛋白药物结合部位的催化转变。

Catalytic transitions in the human MDR1 P-glycoprotein drug binding sites.

机构信息

Department of Biological Sciences, Center for Drug Discovery, Design and Delivery at Dedman College, and Center for Scientific Computation, Southern Methodist University, Dallas, Texas 75275-0376, USA.

出版信息

Biochemistry. 2012 Jun 26;51(25):5125-41. doi: 10.1021/bi300299z. Epub 2012 Jun 12.

Abstract

Multidrug resistance proteins that belong to the ATP-binding cassette family like the human P-glycoprotein (ABCB1 or Pgp) are responsible for many failed cancer and antiviral chemotherapies because these membrane transporters remove the chemotherapeutics from the targeted cells. Understanding the details of the catalytic mechanism of Pgp is therefore critical to the development of inhibitors that might overcome these resistances. In this work, targeted molecular dynamics techniques were used to elucidate catalytically relevant structures of Pgp. Crystal structures of homologues in four different conformations were used as intermediate targets in the dynamics simulations. Transitions from conformations that were wide open to the cytoplasm to transition state conformations that were wide open to the extracellular space were studied. Twenty-six nonredundant transitional protein structures were identified from these targeted molecular dynamics simulations using evolutionary structure analyses. Coupled movement of nucleotide binding domains (NBDs) and transmembrane domains (TMDs) that form the drug binding cavities were observed. Pronounced twisting of the NBDs as they approached each other as well as the quantification of a dramatic opening of the TMDs to the extracellular space as the ATP hydrolysis transition state was reached were observed. Docking interactions of 21 known transport ligands or inhibitors were analyzed with each of the 26 transitional structures. Many of the docking results obtained here were validated by previously published biochemical determinations. As the ATP hydrolysis transition state was approached, drug docking in the extracellular half of the transmembrane domains seemed to be destabilized as transport ligand exit gates opened to the extracellular space.

摘要

多药耐药蛋白属于 ATP 结合盒家族,如人类 P-糖蛋白(ABCB1 或 Pgp),是许多癌症和抗病毒化疗失败的原因,因为这些膜转运蛋白将化疗药物从靶细胞中去除。因此,了解 Pgp 的催化机制细节对于开发可能克服这些耐药性的抑制剂至关重要。在这项工作中,使用靶向分子动力学技术来阐明 Pgp 的催化相关结构。将四种不同构象的同源晶体结构用作动力学模拟中的中间目标。研究了从细胞质到细胞外空间开放的过渡状态构象的宽开放构象的转变。从这些靶向分子动力学模拟中使用进化结构分析鉴定了 26 个非冗余过渡蛋白结构。观察到形成药物结合腔的核苷酸结合域(NBD)和跨膜域(TMD)的耦合运动。观察到 NBD 相互接近时明显的扭曲,以及当到达 ATP 水解过渡态时 TMD 向细胞外空间的剧烈打开的定量。用每个 26 个过渡结构分析了 21 种已知的转运配体或抑制剂的对接相互作用。这里获得的许多对接结果通过先前发表的生化测定得到了验证。随着 ATP 水解过渡态的临近,跨膜域的细胞外半部分的药物对接似乎变得不稳定,因为转运配体出口门向细胞外空间打开。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/628e/3383123/cf1be310f1fc/bi-2012-00299z_0003.jpg

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