Lgi3-4 proteins modulate the KV1.5 channelosome and are potential therapeutic targets for atrial fibrillation

20260 citationsJournal Articlehybrid Open Access

Authors

Paula G. Socuéllamos · Instituto de Investigaciones Biomédicas Sols-Morreale

Álvaro Macías · Spanish National Centre for Cardiovascular Research

Ángela de Benito-Bueno · Instituto de Investigaciones Biomédicas Sols-Morreale

Francisco M. Cruz · Spanish National Centre for Cardiovascular Research

María Redondo-Moya · Instituto de Investigaciones Biomédicas Sols-Morreale

María José Coronado · Hospital Universitario Puerta de Hierro Majadahonda

Abstract

We conclude that Lgi3-4 proteins are new components of the cardiac KV1.5 channelosome. They modulate IKur by interfering with the KV1.5-KVβ interaction. Significantly, Lgi4 is dysregulated differently in paroxysmal vs. permanent AF. The results identify Lgi3-4 proteins as novel regulators of the KV1.5 channelosome, opening new pathways for investigating the role of IKur dysfunction in the mechanism of atrial fibrillation.

Topics & Keywords

interferon and immune responses Endoplasmic Reticulum Stress and Disease Immune Cell Function and Interaction

Publication Details

Published in: Cardiovascular Research

DOI: 10.1093/cvr/cvag049

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Lgi3-4 proteins modulate the KV1.5 channelosome and are potential therapeutic targets for atrial fibrillation

Authors

Abstract

Topics & Keywords

Publication Details