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1
Targeting of DNA gyrase in Streptococcus pneumoniae by sparfloxacin: selective targeting of gyrase or topoisomerase IV by quinolones.司帕沙星对肺炎链球菌中DNA回旋酶的靶向作用：喹诺酮类药物对回旋酶或拓扑异构酶IV的选择性靶向作用
Antimicrob Agents Chemother. 1997 Feb;41(2):471-4. doi: 10.1128/AAC.41.2.471.
2
DNA gyrase and topoisomerase IV are dual targets of clinafloxacin action in Streptococcus pneumoniae.DNA 回旋酶和拓扑异构酶IV是环丙沙星作用于肺炎链球菌的双重靶点。
Antimicrob Agents Chemother. 1998 Nov;42(11):2810-6. doi: 10.1128/AAC.42.11.2810.
3
Potent antipneumococcal activity of gemifloxacin is associated with dual targeting of gyrase and topoisomerase IV, an in vivo target preference for gyrase, and enhanced stabilization of cleavable complexes in vitro.吉米沙星强大的抗肺炎球菌活性与对回旋酶和拓扑异构酶IV的双重靶向作用、在体内对回旋酶的靶点偏好以及在体外增强可裂解复合物的稳定性有关。
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4
Quinolone resistance mutations in Streptococcus pneumoniae GyrA and ParC proteins: mechanistic insights into quinolone action from enzymatic analysis, intracellular levels, and phenotypes of wild-type and mutant proteins.肺炎链球菌GyrA和ParC蛋白中的喹诺酮耐药性突变：基于酶分析、细胞内水平以及野生型和突变型蛋白表型对喹诺酮作用机制的深入了解
Antimicrob Agents Chemother. 2001 Nov;45(11):3140-7. doi: 10.1128/AAC.45.11.3140-3147.2001.
5
Cloning and characterization of the parC and parE genes of Streptococcus pneumoniae encoding DNA topoisomerase IV: role in fluoroquinolone resistance.肺炎链球菌编码DNA拓扑异构酶IV的parC和parE基因的克隆与特性分析：在氟喹诺酮耐药性中的作用
J Bacteriol. 1996 Jul;178(14):4060-9. doi: 10.1128/jb.178.14.4060-4069.1996.
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Sparfloxacin resistance in clinical isolates of Streptococcus pneumoniae: involvement of multiple mutations in gyrA and parC genes.肺炎链球菌临床分离株对司帕沙星的耐药性：gyrA和parC基因中多个突变的作用
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Engineering the specificity of antibacterial fluoroquinolones: benzenesulfonamide modifications at C-7 of ciprofloxacin change its primary target in Streptococcus pneumoniae from topoisomerase IV to gyrase.设计抗菌氟喹诺酮类药物的特异性：环丙沙星C-7位的苯磺酰胺修饰将其在肺炎链球菌中的主要靶点从拓扑异构酶IV转变为回旋酶。
Antimicrob Agents Chemother. 2000 Feb;44(2):320-5. doi: 10.1128/AAC.44.2.320-325.2000.
8
Contribution of topoisomerase IV and DNA gyrase mutations in Streptococcus pneumoniae to resistance to novel fluoroquinolones.肺炎链球菌中拓扑异构酶IV和DNA促旋酶突变对新型氟喹诺酮类药物耐药性的影响
Antimicrob Agents Chemother. 1999 Aug;43(8):2000-4. doi: 10.1128/AAC.43.8.2000.
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Primary targets of fluoroquinolones in Streptococcus pneumoniae.肺炎链球菌中氟喹诺酮类药物的主要作用靶点。
Antimicrob Agents Chemother. 1999 Feb;43(2):410-2. doi: 10.1128/AAC.43.2.410.
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High-level fluoroquinolone resistance in Streptococcus pneumoniae requires mutations in parC and gyrA.肺炎链球菌对高水平氟喹诺酮类药物耐药需要parC和gyrA发生突变。
Antimicrob Agents Chemother. 1996 Dec;40(12):2760-4. doi: 10.1128/AAC.40.12.2760.

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本文引用的文献

1
Involvement of topoisomerase IV and DNA gyrase as ciprofloxacin targets in Streptococcus pneumoniae.拓扑异构酶IV和DNA促旋酶作为环丙沙星在肺炎链球菌中的作用靶点。
Antimicrob Agents Chemother. 1996 Oct;40(10):2321-6. doi: 10.1128/AAC.40.10.2321.
2
Quinolone-resistant mutants of escherichia coli DNA topoisomerase IV parC gene.大肠杆菌DNA拓扑异构酶IV parC基因的喹诺酮抗性突变体
Antimicrob Agents Chemother. 1996 Mar;40(3):710-14. doi: 10.1128/AAC.40.3.710.
3
Genetic evidence for a role of parC mutations in development of high-level fluoroquinolone resistance in Escherichia coli.关于parC突变在大肠杆菌高水平氟喹诺酮耐药性形成中作用的遗传学证据。
Antimicrob Agents Chemother. 1996 Apr;40(4):879-85. doi: 10.1128/AAC.40.4.879.
4
Quinolone resistance mutations in topoisomerase IV: relationship to the flqA locus and genetic evidence that topoisomerase IV is the primary target and DNA gyrase is the secondary target of fluoroquinolones in Staphylococcus aureus.拓扑异构酶IV中的喹诺酮耐药性突变：与flqA位点的关系以及金黄色葡萄球菌中拓扑异构酶IV是氟喹诺酮类药物的主要靶点而DNA回旋酶是次要靶点的遗传学证据。
Antimicrob Agents Chemother. 1996 Aug;40(8):1881-8. doi: 10.1128/AAC.40.8.1881.
5
Cloning and characterization of the parC and parE genes of Streptococcus pneumoniae encoding DNA topoisomerase IV: role in fluoroquinolone resistance.肺炎链球菌编码DNA拓扑异构酶IV的parC和parE基因的克隆与特性分析：在氟喹诺酮耐药性中的作用
J Bacteriol. 1996 Jul;178(14):4060-9. doi: 10.1128/jb.178.14.4060-4069.1996.
6
Alterations in the DNA topoisomerase IV grlA gene responsible for quinolone resistance in Staphylococcus aureus.负责金黄色葡萄球菌喹诺酮耐药性的DNA拓扑异构酶IV grlA基因的改变。
Antimicrob Agents Chemother. 1996 May;40(5):1157-63. doi: 10.1128/AAC.40.5.1157.
7
In vitro activity of fluoroquinolones against gram-positive bacteria.氟喹诺酮类药物对革兰氏阳性菌的体外活性。
Drugs. 1995;49 Suppl 2:48-57. doi: 10.2165/00003495-199500492-00009.
8
The role of new quinolones in the treatment of respiratory tract infections.新型喹诺酮类药物在呼吸道感染治疗中的作用。
Drugs. 1995;49 Suppl 2:144-51. doi: 10.2165/00003495-199500492-00024.
9
Topoisomerase IV is a target of quinolones in Escherichia coli.拓扑异构酶IV是喹诺酮类药物在大肠杆菌中的作用靶点。
Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11801-5. doi: 10.1073/pnas.92.25.11801.
10
New quinolones and gram-positive bacteria.新型喹诺酮类药物与革兰氏阳性菌
Antimicrob Agents Chemother. 1994 Feb;38(2):163-9. doi: 10.1128/AAC.38.2.163.

司帕沙星对肺炎链球菌中DNA回旋酶的靶向作用：喹诺酮类药物对回旋酶或拓扑异构酶IV的选择性靶向作用

Targeting of DNA gyrase in Streptococcus pneumoniae by sparfloxacin: selective targeting of gyrase or topoisomerase IV by quinolones.

作者信息

Pan X S, Fisher L M

机构信息

Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, University of London, United Kingdom.

出版信息

Antimicrob Agents Chemother. 1997 Feb;41(2):471-4. doi: 10.1128/AAC.41.2.471.

DOI:10.1128/AAC.41.2.471
PMID:9021211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC163733/
Abstract

gyrA and parC mutations have been identified inn Streptococcus pneumoniae mutants stepwise selected for resistance to sparfloxacin, an antipneumococcal fluoroquinolone. GyrA mutations (at the position equivalent to resistance hot spot Ser-83 in Escherichia coli GyrA) were found in all 17 first-step mutants examined and preceded DNA topoisomerase IV parC mutations (at Ser-79 or Glu-83), which appeared only in second-step mutants. The targeting of gyrase by sparfloxacin in S. pneumoniae but of topoisomerase IV by ciprofloxacin indicates that target preference can be altered by changes in quinolone structure.

摘要

在逐步选择对抗肺炎球菌氟喹诺酮类药物司帕沙星耐药的肺炎链球菌突变体中，已鉴定出gyrA和parC突变。在所有检测的17个第一步突变体中均发现了GyrA突变（位于与大肠杆菌GyrA中耐药热点Ser-83等效的位置），且该突变先于DNA拓扑异构酶IV的parC突变（位于Ser-79或Glu-83）出现，后者仅出现在第二步突变体中。司帕沙星在肺炎链球菌中靶向gyrase，而环丙沙星靶向拓扑异构酶IV，这表明喹诺酮结构的改变可改变靶点偏好性。