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。 我们正在开发一种被困在细胞内质网（ER）中的突变M1毒蕈碱受体。 添加药理学伴侣会诱导ER出口和质膜上功能性受体的稳定表达。 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探索其对质膜的运输。 最终，我们希望在原代细胞中表达这种突变受体，并在更自然的情况下研究其功能和运输。