1991/08/01 by Hisahiro Yoshida, M Bogaki, Mami Nakamura +2 · 2 citations
Biochemistry, Genetics and Molecular Biology · #Cancer therapeutics and mechanisms #Antibiotic Resistance in Bacteria #DNA and Nucleic Acid Chemistry
paper · doi:10.1128/aac.35.8.1647
openalex publication_date 1991/08/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/15
Thirteen spontaneous quinolone-resistant gyrB mutants of Escherichia coli KL16, including two that were examined previously, were divided into two types according to their quinolone resistance patterns. Type 1 mutants were resistant to all the quinolones tested, while type 2 mutants were resistant to acidic quinolones and were hypersusceptible to amphoteric quinolones. Nucleotide sequence analysis disclosed that all nine type 1 mutants had a point mutation from aspartic acid to asparagine at amino acid 426 and that all four type 2 mutants had a point mutation from lysine to glutamic acid at amino acid 447.