PEPTIDOGLYCAN ANALYSIS OF VSE AND VRE

VSE 和 VRE 的肽聚糖分析

• 批准号: 8168728
• 负责人: JACOB SCHAEFER
• 金额: $ 2.12万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-03-10 至 2010-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8168728
• 关键词: Anabolism; Antibiotics; Binding Sites; Categories; Cell Death; Cell Wall; Computer Retrieval of Information on Scientific Projects Database; Enterococcus; Enterococcus faecium; Funding; Glycopeptides; Grant; Hospitals; Human; Incidence; Infection; Institution; Penicillins; Peptidoglycan; Pharmaceutical Preparations; Problem Solving; Research; Research Personnel; Resistance; Resort; Resources; Source; United States National Institutes of Health; Vancomycin; pathogen

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. Enterococcus faecium, an opportunistic pathogen, causes a substantial proportion of enterococcal human infections, particularly in hospitals. Due to the intrinsic resistance that enterococci demonstrate towards many categories of antibiotics (e.g., penicillins), the most successful treatment has been glycopeptides. Glycopeptides cause bacterial cell death by perturbing the integrity of the cell wall. The most powerful glycopeptide, the so-called "drug of last resort," is vancomycin. However, the incidence of infections resistant to vancomycin has increased rapidly since 1988. Solving the problem of enterococcal resistance requires an understanding of the biosynthesis and organization of the cell-wall peptidoglycan, a potential binding site of vancomycin.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 粪肠球菌是一种机会致病菌，在人类感染中占相当大的比例，尤其是在医院。由于肠球菌对许多种类的抗生素(如青霉素)表现出内在的耐药性，最成功的治疗方法是糖肽。糖肽通过扰乱细胞壁的完整性导致细菌细胞死亡。最强的糖肽，也就是所谓的“最后的药物”，就是万古霉素。然而，自1988年以来，对万古霉素耐药的感染发生率迅速上升。解决肠球菌耐药性的问题需要了解细胞壁肽聚糖的生物合成和组织，它是万古霉素的潜在结合部位。