FUNCTION AND REGULATION OF COP9 SIGNALOSOME

COP9 信号体的功能和调控

• 批准号: 8171230
• 负责人: RAYMOND J DESHAIES
• 金额: $ 0.24万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-09-01 至 2011-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8171230
• 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的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 COP 9信号体（CSN）在调节cullin-RING泛素连接酶（CRL）的活性中起关键作用。 CSN的工作原理是从CRL的cullin亚基上切割泛素样蛋白Nedd 8。 我们试图了解CSN如何工作，以及它的活动是如何控制的。 我们解决这些问题的策略之一是亲和纯化来自不同来源的CSN，包括酵母和人细胞，并通过多维质谱法评估与CSN共沉淀的多肽。