ANTIBIOTIC RESISTANCE MUTATIONS IN H MARISMORTUI 50S RIBOSOMAL SUBUNITS

H MARISMORTUI 50S 核糖体亚基中的抗生素耐药性突变

• 批准号: 7602291
• 负责人: PETER B. MOORE
• 金额: $ 0.58万
• 依托单位: BROOKHAVEN SCIENCE ASSOC-BROOKHAVEN LAB
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7602291
• 关键词: 13-deoxytedanolide; Anisomycin; Antibiotic Resistance; Antibiotics; Binding Sites; Chloramphenicol; Computer Retrieval of Information on Scientific Projects Database; DNA Sequence Rearrangement; Distant; Drug Binding Site; Funding; Grant; Institution; Mutation; Object Attachment; Peptides; Pharmaceutical Preparations; Point Mutation; Protein Biosynthesis; RNA; Research; Research Personnel; Resistance; Resources; Source; Structure; Testing; United States National Institutes of Health; base; negamycin; novel; research study

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Structures of H. marismortui 50S ribosomal subunits containing antibitoic resistance mutations for chloramphenicol and anisomycin will be studied. The RNA point mutations do not occur immediately at the known binding sites for either drug, but occur one or more bases distant to the antibiotic binding site. Thus these experiments will test the hypothesis that subtle structural rearrangements may maintain features necessary for peptide bond formation but change the binding site for the drug. Novel antibiotics girolline, negamycin, and 13-deoxytedanolide, which have previously unidentified binding sites and unknown mechanisms of inhibiting protein synthesis termination will also be studied.

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