自身抗肿瘤抗生素抗性：一种 DNA 糖基化酶在崖霉素生物合成中触发碱基切除修复系统。
Self-resistance to an antitumor antibiotic: a DNA glycosylase triggers the base-excision repair system in yatakemycin biosynthesis.
机构信息
State Key Laboratory of Bioorganic and Natural Products Chemistry, Chinese Academy of Sciences, China.
出版信息
Angew Chem Int Ed Engl. 2012 Oct 15;51(42):10532-6. doi: 10.1002/anie.201204109. Epub 2012 Sep 17.
PMID:22987648
Abstract
Resistance is (not) futile: The yatakemycin biosynthetic gene cluster involves the ytkR2 gene, which encodes a protein with homology to a recently discovered bacterial DNA glycosylase. Genetic validation in vivo, biochemical assays, and in vitro mutagenesis studies revealed that YtkR2 confers resistance for the bacteria by specifically recognizing and cleaving the YTM-modified base (see scheme).
摘要
抵抗并非徒劳
雅他霉素生物合成基因簇涉及 ytkR2 基因，该基因编码与最近发现的细菌 DNA 糖苷酶具有同源性的蛋白质。体内遗传验证、生化分析和体外诱变研究表明，YtkR2 通过特异性识别和切割 YTM 修饰碱基赋予细菌抗性（见方案）。
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