Jeong Jin-Yong, Kim Eun Sil, Choi Sang-Ho, Kwon Hyun-Hee, Lee Sang-Rok, Lee Sang-Oh, Kim Mi-Na, Woo Jun Hee, Kim Yang Soo
Division of Infectious Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
Diagn Microbiol Infect Dis. 2008 Jan;60(1):105-7. doi: 10.1016/j.diagmicrobio.2007.07.015. Epub 2007 Sep 21.
The qnrA1 gene was cloned into a plasmid vector and transformed into Escherichia coli strains carrying chromosomal mutations in the acrAB drug efflux system. In acrAB-deleted strains, and in strains overexpressing acrAB, viable qnrA conferred higher MIC levels (at least a 32-fold increase) for fluoroquinolones than were observed in the parent strains.
qnrA1基因被克隆到质粒载体中,并转化到携带acrAB药物外排系统染色体突变的大肠杆菌菌株中。在缺失acrAB的菌株以及过表达acrAB的菌株中,有活力的qnrA使氟喹诺酮类药物的最低抑菌浓度(MIC)水平比亲本菌株中观察到的水平更高(至少增加32倍)。