FANCONI ANEMIA I AND D2 COMPLEX

FANCONI 贫血 I 和 D2 复合物

• 批准号: 8170595
• 负责人: NIKOLA PAVLETICH
• 金额: $ 0.27万
• 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/8170595
• 关键词: Affect; Anemia; Complex; Computer Retrieval of Information on Scientific Projects Database; DNA Repair; Event; Fanconi' s Anemia; Funding; Grant; Hereditary Disease; Incidence; Individual; Institution; Lesion; Malignant Neoplasms; Molecular; Mono-S; Mutation; Pathway interactions; Process; Proteins; Research; Research Personnel; Resources; Solid Neoplasm; Source; Ubiquitination; United States National Institutes of Health; base; crosslink; disease phenotype; leukemia; repaired

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. Fanconia Anemia (FA) is a genetic disease that predisposes individuals to incidences of cancer, including leukemia and solid tumors. Moreover, some of FA gene products interact with the components of the BRCA pathway. The key downstream components in the FA pathway are the FA-I and FA-D2 gene products, whose mono-ubiquitinations are thought to be a key event in the repair process. Mutations that affect the mono-ubiquitination of these products or disrupting obligatory association between the two proteins are thought to be causative factors for the disease phenotypes. Thus, structural information for the FA-I/D2 complex is critical in assessing the molecular basis for FA-related cancers and elucidate the DNA repair mechanisms of cross-link and double-stranded break lesions.

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