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

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。 我们正在开发一种突变的M1毒碱受体，它被困在细胞的内质网(ER)中。添加一个药理伴侣可诱导内质网退出并稳定表达质膜上的全功能受体。我们已经制作了该突变体的GFP融合蛋白，并希望利用TIRF在稳定表达该突变体的细胞中探索其向质膜的转运。最终，我们希望在原代细胞中表达这种突变的受体，并在更自然的背景下研究它的功能和运输。

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.