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

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH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。 添加药理学伴侣诱导ER退出和质膜上全功能受体的稳定表达。 我们已经做了这个突变体的GFP融合蛋白，并希望探索其运输到质膜使用TIRF细胞稳定表达这种突变体。 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。

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.