NCB5OR DEFICIENCY INCREASES FATTY ACID CATABOLISM, OXIDATIVE STRESS

NCB5OR 缺乏会增加脂肪酸分解代谢和氧化应激

• 批准号: 8361462
• 负责人: Hao Zhu
• 金额: $ 0.81万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361462
• 关键词: Age; Catabolism; Cells; Cytochromes b5; Diabetes Mellitus; Endoplasmic Reticulum; Fatty Acids; Funding; Grant; Hepatocyte; Lipoatrophy; Mass Spectrum Analysis; Mus; NADH; National Center for Research Resources; Oxidation-Reduction; Oxidative Stress; Oxidoreductase; Predisposition; Principal Investigator; Proteins; Research; Research Infrastructure; Resources; Saturated Fatty Acids; Source; Streptozocin; Toxin; United States National Institutes of Health; animal tissue; biomedical resource; cost; cytotoxic

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. NADH cytochrome b5 oxidoreductase (Ncb5or) is an endoplasmic reticulum-associated redox protein that is widely distributed in animal tissues. Ncb5or-/- mice develop diabetes at age 7 weeks and have increased susceptibility to the diabetogenic effects of the b-cell toxin streptozotocin. Ncb5or deficiency also results in lipoatrophy and increased hepatocyte sensitivity to cytotoxic effects of saturated fatty acids.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 NADH细胞色素b5氧化还原酶（Ncb5or）是一种广泛分布于动物组织中的内质网相关氧化还原蛋白。 Ncb5or-/- 小鼠在 7 周龄时患上糖尿病，并且对 b 细胞毒素链脲佐菌素的糖尿病作用的易感性增加。 Ncb5or 缺乏还会导致脂肪萎缩和肝细胞对饱和脂肪酸细胞毒性作用的敏感性增加。