FRUCTOSE-6-PHOSPHATE KINASE

6-磷酸果糖激酶

• 批准号: 8170664
• 负责人: JURGEN SYGUSCH
• 金额: $ 0.29万
• 依托单位: BROOKHAVEN SCIENCE ASSOC-BROOKHAVEN LAB
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8170664
• 关键词: Advanced Glycosylation End Products; Alzheimer' s Disease; Bacteria; Biological Models; Blood Circulation; Cardiovascular Diseases; Catalysis; Chronic Disease; Complex; Computer Retrieval of Information on Scientific Projects Database; Crystallization; Enzymes; Escherichia coli; Fructose; Funding; Galactose; Glucose; Grant; Institution; Malignant Neoplasms; Non-Insulin-Dependent Diabetes Mellitus; Pathway interactions; Phosphotransferases; Proteins; Reaction; Research; Research Personnel; Resolution; Resources; Series; Source; Structure; United States National Institutes of Health; age related; deafness; fructose-6-phosphate; glycation; milligram; repair enzyme; sensory neuropathy; sugar

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. Glycation is the reaction of glucose, fructose, or galactose with proteins that occurs primarily in the bloodstream and is the first step in a complex series of very slow reactions in the body leading to advanced glycation endproducts (AGEs). AGEs are frequently more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases including: type II diabetes, cardiovascular diseases, Alzheimer's disease, cancer, peripheral neuropathy, and sensory losses such as deafness and blindness.Deglycation enzymes repair the initial damage caused by glycation. At present very little is known about the structure of deglycation enzymes, how they recognize glycated proteins, and how they catalyse deglycation. As a model system, several enzymes that are involved in deglycation reactions in E. coli bacteria have been cloned, expressed and purified in milligrams amounts. Screens have identified crystallization conditions for several of these enzymes and are awaiting diffraction analyses for structure determination. One of these, the structure of a fructose-6-phosphate kinase which catalysis the first step in a deglycation pathway was recently solved to 2.1A resolution and is subject of on-going structural study.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 糖化是葡萄糖、果糖或半乳糖与蛋白质的反应，主要发生在血液中，是体内一系列复杂的非常缓慢的反应的第一步，导致晚期糖基化终产物 (AGE)。 AGE 通常比其来源的糖更具反应性，并且与许多与年龄相关的慢性疾病有关，包括：II 型糖尿病、心血管疾病、阿尔茨海默病、癌症、周围神经病变以及耳聋和失明等感觉丧失。酶修复糖化引起的初始损伤。目前，人们对去糖化酶的结构、它们如何识别糖化蛋白以及它们如何催化去糖化知之甚少。作为模型系统，几种参与大肠杆菌去糖化反应的酶已被克隆、表达并以毫克级纯化。筛选已经确定了其中几种酶的结晶条件，并正在等待衍射分析以确定结构。其中之一是果糖 6 磷酸激酶的结构，该激酶催化去糖化途径的第一步，最近已分辨率达到 2.1A，并且是正在进行的结构研究的主题。