PEPTIDOGLYCAN ANALYSIS OF VSE AND VRE

VSE 和 VRE 的肽聚糖分析

• 批准号: 7953960
• 负责人: JACOB SCHAEFER
• 金额: $ 1.86万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-02-01 至 2010-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7953960
• 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; Mass Spectrum Analysis; Penicillins; Peptidoglycan; Pharmaceutical Preparations; Problem Solving; Research; Research Personnel; Resistance; Resort; Resources; Source; United States National Institutes of Health; Vancomycin; biomedical resource; 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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。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。列出的机构是 对于中心，这不一定是调查员的机构。 机会性病原体肠球菌引起了很大一部分肠球菌的感染，尤其是在医院。 由于肠球菌对许多类别的抗生素（例如青霉素）的固有抗性，最成功的治疗方法是糖肽。 糖肽通过扰动细胞壁的完整性引起细菌细胞死亡。 万古霉素是最强大的糖肽，即所谓的“最后手段”。 然而，自1988年以来，抗性万古霉素的感染发生率已迅速增加。解决肠球菌耐药性问题需要了解细胞壁肽聚糖的生物合成和组织，这是Vancomycin的潜在结合位点。