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Differential Glycosylation of the Inwardly Rectifying Potassium Channel Kir7.1 by G Protein-Coupled Receptors
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| 자료유형 | 학위논문 |
|---|---|
| 서명/저자사항 | Differential Glycosylation of the Inwardly Rectifying Potassium Channel Kir7.1 by G Protein-Coupled Receptors. |
| 개인저자 | Carrington, Sheridan J. S. |
| 단체저자명 | Vanderbilt University. Molecular Physiology and Biophysics. |
| 발행사항 | [S.l.]: Vanderbilt University., 2019. |
| 발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2019. |
| 형태사항 | 114 p. |
| 기본자료 저록 | Dissertations Abstracts International 81-03B. Dissertation Abstract International |
| ISBN | 9781088320099 |
| 학위논문주기 | Thesis (Ph.D.)--Vanderbilt University, 2019. |
| 일반주기 |
Source: Dissertations Abstracts International, Volume: 81-03, Section: B.
Advisor: Colbran, Roger J. |
| 이용제한사항 | This item must not be sold to any third party vendors. |
| 요약 | Kir7.1 is an inwardly rectifying potassium channel with important roles in the regulation of the membrane potential in retinal pigment epithelium, uterine smooth muscle, and hypothalamic neurons. Regulation of G protein-coupled inwardly rectifying potassium (GIRK) channels by G protein-coupled receptors (GPCRs) via the G protein beta gamma subunits has been well characterized. However, how Kir channels are regulated is incompletely understood. We report here that Kir7.1 is also regulated by GPCRs, but through a different mechanism. Using Western blot analysis, we observed that multiple GPCRs tested caused a striking reduction in the complex glycosylation of Kir7.1. Further, GPCR-mediated reduction of Kir7.1 glycosylation in HEK293T cells did not alter its expression at the cell surface but decreased channel activity. Of note, mutagenesis of the sole Kir7.1 glycosylation site reduced conductance and open probability, as indicated by single-channel recording. Additionally, we report that the L241P mutation of Kir7.1 associated with Lebers congenital amaurosis (LCA), an inherited retinal degenerative disease has significantly reduced complex glycosylation. Collectively, these results suggest that Kir7.1 channel glycosylation is essential for function, and this activity within cells is suppressed by most GPCRs. The Melanocortin 4 receptor (MC4R), a GPCR previously reported to induce ligand-regulated activity of this channel, is the only GPCR tested that does not have this effect on Kir7.1. |
| 일반주제명 | Molecular biology. Physiology. |
| 언어 | 영어 |
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