Susceptibility to Neurodegeneration and Birth Defects in Mice with Proofreading-Deficient mitochondrial DNA Polymerase.

线粒体 DNA 聚合酶校对缺陷小鼠对神经退行性变和出生缺陷的易感性。

• 批准号: 201011
• 负责人: Bralha Fernando N
• 金额: $ 1.27万
• 依托单位: University of Toronto
• 依托单位国家: 加拿大
• 项目类别: Studentship Programs
• 财政年份: 2010
• 资助国家: 加拿大
• 起止时间: 2010-02-01 至 2011-02-01
• 项目状态: 已结题
• 来源: https://webapps.cihr-irsc.gc.ca/decisions/p/project_details.html?applId=201011&lang=en
• 关键词: Animal Models; Dna Damage And Repair; Mitochondrial Dna; Neural Stem Cells; Neurodegeneration; Rotenone Toxicology; Teratogenicity

Mitochondria are the "power plant" of the cell because they produce ATP, the cell's energy currency. DNA Polymerase Gamma (Polg) is the enzyme responsible for replicating mitochondrial DNA(mtDNA). When the Polg proofreading activity is missing, DNA mutati

线粒体是细胞的“动力工厂”，因为它们产生细胞的能量货币--三磷酸腺苷。DNA聚合酶(Polg)是负责复制线粒体DNA(MtDNA)的酶。当Polg校对活动缺失时，DNA发生突变