PBP4 Mediates β-Lactam Resistance by Altered Function
PBP4 Mediates β-Lactam Resistance by Altered Function
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DOI：
10.1128/aac.00932-17
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发表时间：
2017-11-01
影响因子：
4.9
通讯作者：
Chambers, Henry F.
中科院分区：
文献类型：
--
作者：
Chatterjee, Som S.;Chen, Liang;Chambers, Henry F.
青霉素结合蛋白4（PBP4）可在金黄色葡萄球菌中提供高水平的β-内酰胺耐药性。一系列与pbp4相关的错义和启动子突变在显示高水平耐药的菌株中被检测到。我们发现错义突变促进了PBP4介导的β-内酰胺抗性，启动子突变导致PBP4过表达。我们的研究结果还表明，β-内酰胺耐药的PBPs之间的合作相互作用。
Penicillin binding protein 4 (PBP4) can provide high-level beta-lactam resistance in Staphylococcus aureus. A series of missense and promoter mutations associated with pbp4 were detected in strains that displayed high-level resistance. We show here that the missense mutations facilitate the beta-lactam resistance mediated by PBP4 and the promoter mutations lead to overexpression of pbp4. Our results also suggest a cooperative interplay among PBPs for beta-lactam resistance.