FUNCTION AND REGULATION OF COP9 SIGNALOSOME

COP9 信号体的功能和调控

• 批准号: 7723626
• 负责人: RAYMOND J DESHAIES
• 金额: $ 0.81万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-09-01 至 2009-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7723626
• 关键词: Address; Affinity; Cells; Cleaved cell; Computer Retrieval of Information on Scientific Projects Database; Funding; Grant; Human; Institution; Mass Spectrum Analysis; Play; Regulation; Research; Research Personnel; Resources; Role; Source; Ubiquitin Like Proteins; United States National Institutes of Health; Work; Yeasts; polypeptide; ubiquitin ligase

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. COP9 Signalosome (CSN) plays a critical role in regulating the activity of cullin-RING ubiquitin ligases (CRLs). CSN works by cleaving the ubiquitin-like protein Nedd8 from the cullin subunit of CRLs. We seek to understand how CSN works, and how its activity is controlled. One of our strategies to address these questions is to affinity-purify CSN from different sources including yeast and human cells, and evaluate by multidimensional mass spectrometry the polypeptides that co-precipitate with CSN.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 COP9信号小体(CSN)在调节剔除环泛素连接酶(CRL)活性中起着关键作用。CSN的工作原理是从CRLS的cullin亚单位中切割泛素样蛋白Nedd8。我们试图了解CSN是如何工作的，以及它的活动是如何受到控制的。我们解决这些问题的策略之一是从包括酵母和人类细胞在内的不同来源的CSN中进行亲和纯化，并通过多维质谱对与CSN共沉淀的多肽进行评估。