Biochemical reconstitution of the ubiquitin ligase pathway defective in Fanconi Anaemia

范可尼贫血泛素连接酶途径缺陷的生化重建

• 批准号: nhmrc : 1031104
• 负责人: Dr Andrew Deans
• 金额: $ 37.52万
• 依托单位: St. Vincent's Institute of Medical Research
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2012
• 资助国家: 澳大利亚
• 起止时间: 2012-01-01 至 2014-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/biochemical-reconstitution-ubiquitin-fanconi-anaemia/110788
• 关键词: Biochemical; reconstitution; ubiquitin; ligase; pathway

Fanconi Anemia (FA) is characterised by loss of vital blood cells but also 700x risk of developing leukaemia and other cancers. FA is caused by an inherited defect in one of 15 different genes that provide a signal and repair mechanism protecting cells from cancer causing mutations. By reconstructing this signaling mechanism in the test tube we will determine how it contributes to cancer protection, and highlight potential strategies for treatment of FA and leukaemia in the general population.

范可尼贫血(FA)的特征是失去重要的血细胞，但患白血病和其他癌症的风险也是700倍。FA是由15种不同基因中的一种遗传缺陷引起的，这些基因提供了一种信号和修复机制，保护细胞免受癌症引起的突变。通过在试管中重建这种信号机制，我们将确定它如何有助于癌症保护，并强调在普通人群中治疗FA和白血病的潜在策略。