Stp1 功能丧失促进金黄色葡萄球菌对β-内酰胺类抗生素的耐药性，且与经典基因无关。
Stp1 Loss of Function Promotes β-Lactam Resistance in Staphylococcus aureus That Is Independent of Classical Genes.
机构信息
Department of Microbial Pathogenesis, School of Dentistry, University of Maryland and Institute of Marine and Environmental Technology, Baltimore, Maryland, USA.
Department of Microbial Pathogenesis, School of Dentistry, University of Maryland and Institute of Marine and Environmental Technology, Baltimore, Maryland, USA
出版信息
Antimicrob Agents Chemother. 2020 May 21;64(6). doi: 10.1128/AAC.02222-19.
Abstract
β-Lactam resistance in limits treatment options. Stp1 and Stk1, a serine-threonine phosphatase and kinase, respectively, mediate serine-threonine kinase (STK) signaling. Loss-of-function point mutations in were detected among laboratory-passaged β-lactam-resistant strains lacking and , the major determinants of β-lactam resistance in the bacteria. Loss of Stp1 function facilitates β-lactam resistance of the bacteria.
摘要
β-内酰胺耐药限制了治疗选择。Stp1 和 Stk1 分别是一种丝氨酸-苏氨酸磷酸酶和激酶，介导丝氨酸-苏氨酸激酶 (STK) 信号转导。在缺乏细菌中主要的β-内酰胺耐药决定因子 blaNDM-1 和 blaCTX-M-15 的实验室传代β-内酰胺耐药株中检测到 点突变。Stp1 功能丧失促进了细菌的β-内酰胺耐药性。
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