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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom