ROLE OF THE MRE11/RAD50/NBS1 COMPLEX IN DNA DAMAGE RESPONSE PATHWAYS

MRE11/RAD50/NBS1 复合物在 DNA 损伤反应途径中的作用

• 批准号: 7957690
• 负责人: Xiaohua Wu
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2010-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957690
• 关键词: Affect; Ataxia; Biology; Complex; Computer Retrieval of Information on Scientific Projects Database; DNA Damage; Disease; Event; Funding; Fungal Genome; Genome; Genome Stability; Grant; Institution; Link; Maintenance; Malignant Neoplasms; Mediating; Nijmegen Breakage Syndrome; Pathway interactions; Patients; Phase; Prevention; Research; Research Personnel; Resources; Role; Source; Telangiectasis; United States National Institutes of Health; protein complex; response

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. Nbs1 and Mre11 are linked to the Nijmegen breakage syndrome (NBS) and ataxia-telangiectasia-like disorder (ATLD), respectively, and the affected patients are predisposed to cancer. Mre11, Nbs1 and Rad50 form a conserved protein complex that is required for the maintenance of genome stability. Recent studies have also uncovered new roles of MRN in S-phase related events, such as replication control, replication checkpoint and prevention of DSB formation in S-phase, but detailed mechanisms are not clear. We propose to investigate the mechanisms underlying the critical roles of the Mre11/Rad50/Nbs1 complex (MRN) in preserving genome integrity, especially in mediating S-phase-associated DNA damage responses.

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。 Nbs1 和 Mre11 分别与奈梅亨断裂综合征 (NBS) 和共济失调毛细血管扩张样疾病 (ATLD) 有关，受影响的患者容易患癌症。 Mre11、Nbs1 和 Rad50 形成维持基因组稳定性所需的保守蛋白复合物。 最近的研究还揭示了MRN在S期相关事件中的新作用，例如复制控制、复制检查点和预防S期DSB形成，但详细机制尚不清楚。 我们建议研究 Mre11/Rad50/Nbs1 复合物 (MRN) 在保持基因组完整性方面的关键作用的机制，特别是在介导 S 期相关的 DNA 损伤反应方面。