TRAFFICKING OF MUSCARINIC RECEPTOR SUBTYPES USING A MUTANT GFP-FUSION PROTEIN

使用突变 GFP 融合蛋白贩运毒蕈碱受体亚型

• 批准号: 8170986
• 负责人: Fred J Ehlert
• 金额: $ 0.18万
• 依托单位: UNIVERSITY OF CALIFORNIA-IRVINE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-08-01 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8170986
• 关键词: Cell membrane; Cells; Chimeric Proteins; Computer Retrieval of Information on Scientific Projects Database; Endoplasmic Reticulum; Funding; Grant; Institution; Molecular Chaperones; Muscarinic Acetylcholine Receptor; Muscarinic M1 Receptor; Research; Research Personnel; Resources; Source; United States National Institutes of Health; mutant; receptor; reticulum cell; 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. We are developing a mutant M1 muscarinic receptor that is trapped in the endoplasmic reticulum (ER) of cells. Addition of a pharmacological chaperone induces ER exit and stable expression of the fully functional receptor on the plasma membrane. We have made a GFP fusion protein of this mutant, and wish to explore its trafficking to the plasma membrane using TIRF in cells stably expressing this mutant. Ultimately, we wish to express this mutant receptor in primary cells and study its function and trafficking in a more natural context.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 中心，不一定是研究者的机构。 我们正在开发一种突变型 M1 毒蕈碱受体，该受体被捕获在细胞的内质网 (ER) 中。 添加药理学伴侣可诱导 ER 退出并在质膜上稳定表达全功能受体。 我们已经制作了该突变体的 GFP 融合蛋白，并希望在稳定表达该突变体的细胞中使用 TIRF 探索其向质膜的运输。 最终，我们希望在原代细胞中表达这种突变受体，并在更自然的环境中研究其功能和运输。