CHARACTERIZATION OF PKA RIIALPHA-INTERACTING PARTNERS

PKA RIIALPHA 相互作用伙伴的表征

• 批准号: 7957813
• 负责人: ANGEL VELASCO
• 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/7957813
• 关键词: Biology; Catalytic Domain; Cell physiology; Complex; Computer Retrieval of Information on Scientific Projects Database; Cyclic AMP-Dependent Protein Kinases; Funding; Fungal Genome; Golgi Apparatus; Grant; Institution; Mammalian Cell; Molecular; Organelles; Proteins; Research; Research Personnel; Resources; Signal Transduction; Site; Source; Subcellular structure; Transport Process; United States National Institutes of Health; interest; transmission process

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. PKA anchoring to subcellular structures is a major issue in cell signalling. The Golgi apparatus is a site of PKA concentration in mammalian cells. Our previous studies indicate that Golgi-associated PKA is involved in the control of transport processes, organelle dynamic organization and signal transmission. Whereas these actions are directly promoted by PKA catalytic subunits the regulatory subunits themselves are responsible of both PKA targeting and integration in complex molecular networks. Thus we are interested in the characterization of proteins that specifically interact with PKA regulatory RIIalpha subunits and to determine the relevance of such interaction for cell physiology.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 PKA锚定在亚细胞结构上是细胞信号传导中的主要问题。高尔基体是哺乳动物细胞中PKA浓度的位点。我们以前的研究表明，高尔基体相关的PKA参与了运输过程，Organelle动态组织和信号传播的控制。尽管这些作用是由PKA催化亚基直接促进的，但调节亚基本身是PKA靶向和复杂分子网络中的整合的原因。因此，我们对特异性与PKA调节性Riialpha亚基的蛋白质的表征感兴趣，并确定这种相互作用与细胞生理学的相关性。