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计算研究野生型和突变型肺炎链球菌青霉素结合蛋白 2B(PBP2B)对β-内酰胺类抗生素的耐药性。

Computational studies on the resistance of penicillin-binding protein 2B (PBP2B) of wild-type and mutant strains of Streptococcus pneumoniae against β-lactam antibiotics.

机构信息

Department of Bioinformatics, School of Life Sciences, Bharathidasan University, Tiruchirappalli 620 024, Tamil Nadu, IndiaDepartment of Zoology, Dharmapuram Gnanambigai Government Arts College (Women), Mayiladuthurai 609 001, Tamil Nadu, IndiaDepartment of Bioinformatics, School of Biotechnology and Health Sciences, Karunya University, Coimbatore 641 114, Tamil Nadu, India.

出版信息

Chem Biol Drug Des. 2013 Sep;82(3):275-89. doi: 10.1111/j.1747-0285.2012.01387.x. Epub 2013 Jul 25.

Abstract

Mutations within transpeptidase domain of penicillin-binding protein 2B of the strains of Streptococcus pneumoniae leads to resistance against β-lactam antibiotics. To uncover the important residues responsible for sensitivity and resistance, the recently determined three dimensional structures of penicillin-binding protein 2B of both wild-type R6 (sensitive) and mutant 5204 (resistant) strains along with the predicted structures of other mutant strains G54, Hungary19A-6 and SP195 were considered for the interaction study with β-lactam antibiotics using induced-fit docking of Schrödinger. Associated binding energies of the complexes and their intermolecular interactions in the binding site clearly show that the wild-type R6 as sensitive, mutant strains 5204 and G54 as highly resistant, and the mutant strains Hungary19A-6 and SP195 as intermediate resistant. The study also reveals that the mutant strains Hungary19A-6 and SP195 exhibit intermediate resistant because of the existence of mutations till the intermediate 538th and 516th positions, respectively, and not till the end of the C-terminus. Furthermore, our investigations show that if the mutations are extended till the end of the C terminus, then the antibiotic resistance of induced-mutated strains increases from intermediate to high as in the strains 5204 and G54. The binding patterns obtained in the study are useful in designing potential inhibitors against multidrug resistant S. pneumoniae.

摘要

青霉素结合蛋白 2B 转肽酶结构域内的突变导致肺炎链球菌对β-内酰胺类抗生素产生耐药性。为了揭示与敏感性和耐药性相关的重要残基,对野生型 R6(敏感)和突变型 5204(耐药)菌株的青霉素结合蛋白 2B 的最近确定的三维结构以及其他突变株 G54、Hungary19A-6 和 SP195 的预测结构进行了考虑,使用 Schrödinger 的诱导拟合对接研究与β-内酰胺类抗生素的相互作用。复合物的结合能及其在结合部位的分子间相互作用清楚地表明,野生型 R6 作为敏感株,突变株 5204 和 G54 作为高度耐药株,突变株 Hungary19A-6 和 SP195 作为中度耐药株。研究还表明,突变株 Hungary19A-6 和 SP195 表现出中度耐药性,是因为突变存在于第 538 位和第 516 位之间,而不是 C 末端。此外,我们的研究表明,如果突变延伸到 C 末端,那么诱导突变菌株的抗生素耐药性会从中度增加到高度,就像 5204 和 G54 菌株一样。研究中获得的结合模式可用于设计针对多药耐药性 S. pneumoniae 的潜在抑制剂。

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