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: 7358926
• 负责人: PETER B. MOORE
• 金额: $ 1.12万
• 依托单位: BROOKHAVEN SCIENCE ASSOC-BROOKHAVEN LAB
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7358926
• 关键词: ANTIBIOTIC; RESISTANCE; MUTATIONS; MARISMORTUI; 50S

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

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。将研究含有氯霉素和砷霉素的含有抗抑制性突变的50S核糖体亚基的结构。 RNA点突变不会立即发生在两种药物的已知结合位点，而是发生在抗生素结合位点的一个或多个碱基。因此，这些实验将检验以下假设：微妙的结构重排可以保持肽键形成所需的特征，但会改变该药物的结合位点。新型抗生素Girolline，Negamycin和13-脱氧胆碱，它们以前具有未识别的结合位点以及抑制蛋白质合成终止的未知机制