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Up-Regulation of Kir2.1 (KCNJ2) by the Serum & Glucocorticoid Inducible SGK3
Author(s) -
Carlos Muñoz,
Tatsiana Pakladok,
Ahmad Almilaji,
Bernat Elvira,
Niels Decher,
Ekaterina Shumilina,
Florian Läng
Publication year - 2014
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000358629
Subject(s) - inward rectifier potassium ion channel , patch clamp , sgk1 , ion channel , kinase , biology , protein kinase a , microbiology and biotechnology , potassium channel , endocrinology , medicine , chemistry , electrophysiology , biochemistry , neuroscience , receptor
The serum & glucocorticoid inducible kinase SGK3, an ubiquitously expressed serine/threonine kinase, regulates a variety of ion channels. It has previously been shown that SGK3 upregulates the outwardly rectifying K(+) channel KV11.1, which is expressed in cardiomyocytes. Cardiomyocytes further express the inward rectifier K(+) channel K(ir)2.1, which contributes to maintenance of resting cell membrane potential. Loss-of-function mutations of KCNJ2 encoding K(ir)2.1 result in Andersen-Tawil syndrome with periodic paralysis, cardiac arrhythmia and dysmorphic features. The present study explored whether SGK3 participates in the regulation of K(ir)2.1.

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