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[革兰氏阴性菌诱导β-内酰胺酶的调控机制研究进展]

[Progress in regulatory mechanism for inducing β-lactamase in Gram-negative bacteria].

作者信息

Xu Chaoyi, Zhang Ting, Cai Jingxiao, Yu Zhiliang, Qiu Juanping, Yin Jianhua

机构信息

College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310014, Zhejiang, China.

出版信息

Sheng Wu Gong Cheng Xue Bao. 2018 Aug 25;34(8):1288-1296. doi: 10.13345/j.cjb.180187.

Abstract

Beta-lactams are the most widely used antibiotics. One of the principle mechanisms for Gram-negative bacteria to resist β-lactams is by producing β-lactamases that degrade β-lactams. This review highlights two regulatory mechanisms for inducing β-lactamase in Gram-negative bacteria. In the ampR-ampC paradigm, the induction of β-lactamase is intimately linked to peptidoglycan recycling. AmpR, a LysR-type transcriptional regulator, plays a central role in regulating expression of β-lactamase. Recent studies found that two-component signal transduction pathway is activated by β-lactams, which in turn induces the expression of β-lactamase. Finally, we discussed the future research directions in β-lactam resistance in Gram-negative bacteria.

摘要

β-内酰胺类是使用最广泛的抗生素。革兰氏阴性菌抵抗β-内酰胺类的主要机制之一是产生可降解β-内酰胺类的β-内酰胺酶。本综述重点介绍了革兰氏阴性菌中诱导β-内酰胺酶的两种调控机制。在ampR-ampC模式中,β-内酰胺酶的诱导与肽聚糖循环密切相关。AmpR是一种LysR型转录调节因子,在调节β-内酰胺酶的表达中起核心作用。最近的研究发现,双组分信号转导途径被β-内酰胺类激活,进而诱导β-内酰胺酶的表达。最后,我们讨论了革兰氏阴性菌β-内酰胺耐药性的未来研究方向。

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