P4: ER TO GOLGI T & VSMC

P4：ER 至高尔基 T

• 批准号: 7610596
• 负责人: GUANGYU WU
• 金额: $ 16.09万
• 依托单位: LSU HEALTH SCIENCES CENTER
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610596
• 关键词: Blood Vessels; Computer Retrieval of Information on Scientific Projects Database; Endoplasmic Reticulum; Funding; Golgi Apparatus; Grant; Institution; Molecular Profiling; Muscle Cells; Neonatal; Rattus; Receptor Signaling; Receptor, Angiotensin, Type 1; Research; Research Personnel; Resources; Role; Smooth Muscle Myocytes; Source; United States National Institutes of Health; Ventricular; beta-2 Adrenergic Receptors; protein expression; trafficking

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. The objective of this project is to determine the role of altered ER-to-Golgi trafficking of angiotensin II type 1 receptor (AT1R) and beta 2 adrenergic receptor (AR) in primary cultures of neonatal rat ventricular myocytes and vascular smooth muscle cells. There are three specific aims. First aim is to define the role of Rab1 and other vesicular transport regulators (Sar1, ARF1, Rab2 and Rab6) in the endoplasmic reticulum-to-Golgi transport. Second aim is to determine if alterations in the ER-to-Golgi transport, as a consequence of manipulating Rab1 function, is involved in receptor signaling. Third Aim is to determine the effect of Rab1 on protein expression profile.

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。 本课题的目的是研究血管紧张素II 1型受体(AT1R)和β2肾上腺素能受体(AR)在原代培养的新生大鼠心肌细胞和血管平滑肌细胞中内质网向高尔基体转运的变化。有三个具体目标。第一个目的是确定Rab1和其他囊泡转运调节因子(Sar1、ARF1、Rab2和Rab6)在内质网到高尔基体转运中的作用。第二个目的是确定作为操纵Rab1功能的结果，内质网到高尔基体转运的变化是否参与了受体信号转导。第三个目的是确定Rab1对蛋白质表达谱的影响。