K+ channel complexes: assembly, trafficking and function

这项研究的长期目标是阐明确保 钾(K+)通道与适当的膜包埋调节亚基组装，以适当地 生理功能。N-糖基化是一种重要的共翻译和翻译后修饰，它促进了 K+通道亚基的组装和运输。阻断KCNE K+调节蛋白糖基化的突变 亚基与遗传和药物引起的心律失常(长QT间期)直接相关 综合症)。因此，本建议的两个目的是研究内质网中K+通道亚单位的糖基化， 高尔基体和质膜：(1)我们将确定K+通道亚单位的分子和细胞基础。 和翻译后N-糖基化。(2)我们将重新设计细胞的糖基，以荧光方式显示K+ 从活细胞中排出。

The long-term goal of this research is to elucidate the molecular and cellular mechanisms that ensure potassium (K+) channels assemble with the appropriate membrane-embedded regulatory subunits for proper physiological function. N-glycosylation is a vital co- and post-translational modification that facilitates the assembly and trafficking of K+ channel subunits. Mutations that block glycosylation of KCNE K+ regulatory subunits have been directly linked to the genetic and drug-induced forms of cardiac arrhythmias (Long QT Syndrome). Accordingly, the two aims of this proposal investigate K+ channel subunit glycosylation in the ER, Golgi and plasma membrane: (1) We will determine the molecular and cellular bases of K+ channel subunit co- and post-translational N-glycosylation. (2) We will reengineer the cell's glycocalyx to fluorescently visualize K+ efflux from living cells.