A target-protection mechanism of antibiotic resistance at atomic resolution: insights into FusB-type fusidic acid resistance.
A target-protection mechanism of antibiotic resistance at atomic resolution: insights into FusB-type fusidic acid resistance.
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DOI：
10.1038/srep19524
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发表时间：
2016-01-19
影响因子：
4.6
通讯作者：
O'Neill AJ
中科院分区：
文献类型：
--
作者：
Tomlinson JH;Thompson GS;Kalverda AP;Zhuravleva A;O'Neill AJ
临床上重要的细菌中的抗生素耐药性可以由与药物靶点物理结合并保护其免受抗生素抑制作用的蛋白质介导。我们在这里提出的第一个详细的结构表征，通过蛋白质-蛋白质相互作用介导的这样的目标保护机制，揭示了FusB夫西地酸抗性蛋白和药物靶标（EF-G）之间形成的复合物的结构，它的作用，以保护。FusB与EF-G的结合诱导EF-G的构象和动力学变化，从而阐明夫西地酸抗性的分子机制。
Antibiotic resistance in clinically important bacteria can be mediated by proteins that physically associate with the drug target and act to protect it from the inhibitory effects of an antibiotic. We present here the first detailed structural characterization of such a target protection mechanism mediated through a protein-protein interaction, revealing the architecture of the complex formed between the FusB fusidic acid resistance protein and the drug target (EF-G) it acts to protect. Binding of FusB to EF-G induces conformational and dynamic changes in the latter, shedding light on the molecular mechanism of fusidic acid resistance.