NCI-H295R cell line as in vitro model of hyperaldosteronism lacks functional KCNJ5 (GIRK4; Kir3.4) channels
Author:
Funder
FoRum
Publisher
Elsevier BV
Subject
Endocrinology,Molecular Biology,Biochemistry
Reference62 articles.
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4. Overexpression of monomeric and multimeric GIRK4 subunits in rat atrial myocytes removes fast desensitization and reduces inward rectification of muscarinic K+ current (IK(ACh)). Evidence for functional homomeric GIRK4 channels;Bender;J. Biol. Chem,2001
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1. Regulation of aldosterone production by ion channels: From basal secretion to primary aldosteronism;Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease;2018-03
2. Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney;Physiological Reviews;2016-10
3. Mutated KCNJ5 activates the acute and chronic regulatory steps in aldosterone production;Journal of Molecular Endocrinology;2016-07
4. Interaction between Angiotensin II and Insulin/IGF-1 Exerted a Synergistic Stimulatory Effect on ERK1/2 Activation in Adrenocortical Carcinoma H295R Cells;International Journal of Endocrinology;2016
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