PMID: 9191093Jun 1, 1997Paper

Cloning and characterization of Kir3.1 (GIRK1) C-terminal alternative splice variants

Brain Research. Molecular Brain Research
C S NelsonC N Allen

Abstract

Southern blot analysis of RT-PCR products from brain and heart revealed multiple products for a C-terminal region of Kir3.1. Sequencing yielded clones for wild-type Kir3.1 and three Kir3.1 C-terminal alternative splice variants, including a unique alternative exon. Two of these variants encoded truncated Kir3.1 molecules. Tissue distribution and electrophysiological characterization of a single truncated variant, Kir3.1(00) were then examined. Kir3.1 channels are gated by G-protein beta gamma-subunits binding to the C-terminal domain, thus, the truncation of Kir3.1(00) removes a major functional domain. When incorporated into heteromeric channels with other family members (Kir3.1, 3.2 or 3.4) several functional changes were observed: (1) Kir3.1(00) changes G-protein activation of Kir3 channels; (2) Kir3.1(00) is restricted in its ability to assemble with other channel subunits as heteromers; and (3) incorporation of Kir3.1(00) into heteromeric channel complexes alters the kinetics of channel re-activation.

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Citations

Mar 14, 2002·Gene·Kevin WickmanDavid E Clapham
Apr 15, 2010·Nature Reviews. Neuroscience·Christian Lüscher, Paul A Slesinger
Dec 22, 2007·Journal of Receptor and Signal Transduction Research·Bibiane SteineckerWolfgang Schreibmayer
Feb 19, 2017·The Journal of Biological Chemistry·Anna N BukiyaAvia Rosenhouse-Dantsker
Sep 29, 2006·Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology·Yu-Ki IwasakiTeruo Takano
May 11, 2017·Scientific Reports·Ezequiel Marron Fernandez de VelascoKevin Wickman

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