Mechanism of G Protein Beta5/ R7-RGS Protein/ R7BP Complex Signal Transduction

G蛋白Beta5/ R7-RGS蛋白/ R7BP复合物信号转导机制

• 批准号: 8553474
• 负责人: WILLIAM F SIMONDS
• 金额: $ 49.46万
• 依托单位: NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8553474
• 关键词: Behavioral; Binding; Binding Proteins; Biological Models; Biology; Brain; Cell Nucleus; Cell membrane; Cells; Complex; Cytosol; Development; Enzymes; Family; GTP-Binding Protein Regulators; GTP-Binding Proteins; Goals; Guanine Nucleotides; Human; Ion Channel; Knockout Mice; Modeling; Mus; Neurons; Neurosecretory Systems; Pattern; Property; Protein Isoforms; RGS Proteins; RNA Splicing; Research Project Grants; Retinal Photoreceptors; Rodent; Role; Signal Transduction; Stimulus; Structure; System; Transcript; Transducers; Work; extracellular; genetic regulatory protein; loss of function; mammalian genome; protein complex; receptor; receptor coupling

The purpose of the current work is to understand the signaling function of the evolutionarily-conserved Gbeta5/R7-RGS/R7BP complex in humans. To this end we are first trying to identify and characterize the functions of the Gbeta5 complex in model systems such as cultured PC12 and SH-SY5Y cells, primary rodent brain neurons, and genetically-modified mice. The effect of the loss-of-function of Gbeta5 and other complex components in neurons and brains of knockout mice is currently being examined using developmental, behavioral, immunohistochemical, and neuroanatomical analyses.

目前的工作的目的是了解人类进化保守的Gbeta 5/R7-RGS/R7 BP复合物的信号功能。 为此，我们首先试图识别和表征Gbeta 5复合物在模型系统中的功能，例如培养的PC 12和SH-SY 5 Y细胞，原代啮齿动物脑神经元和遗传修饰小鼠。 目前正在使用发育，行为，免疫组织化学和神经解剖学分析来研究Gbeta 5和其他复杂成分在敲除小鼠神经元和大脑中功能丧失的影响。