New Adrenal Cortex Hormones Study Results from Queen's University Described (The serum- and glucocorticoid-inducible kinases SGK1 and SGK3 regulate...

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New Adrenal Cortex Hormones Study Results from Queen's University Described (The serum- and glucocorticoid-inducible kinases SGK1 and SGK3 regulate hERG channel expression via ubiquitin ligase Nedd4-2 and GTPase Rab11) By a News Reporter-Staff News Editor at Life Science Weekly -- A new study on Adrenal Cortex Hormones is now available. According to news reporting from Kingston, Canada, by NewsRx journalists, research stated, "The hERG (human ether-a-go-go-related gene) encodes the ? subunit of the rapidly activating delayed rectifier potassium channel (IKr). Dysfunction of hERG channels due to mutations or certain medications causes long QT syndrome, which can lead to fatal ventricular arrhythmias or sudden death." The news correspondents obtained a quote from the research from Queen's University, "Although the abundance of hERG in the plasma membrane is a key determinant of hERG functionality, the mechanisms underlying its regulation are not well understood. In the present study, we demonstrated that overexpression of the stress-responsive serum-and glucocorticoid-inducible kinase (SGK) isoforms SGK1 and SGK3 increased the current and expression level of the membrane-localized mature proteins of hERG channels stably expressed in HEK 293 (hERG-HEK) cells. Furthermore, the synthetic glucocorticoid, dexamethasone, increased the current and abundance of mature ERG proteins in both hERG-HEK cells and neonatal cardiac myocytes through the enhancement of SGK1 but not SGK3 expression. We have previously shown that mature hERG channels are degraded by ubiquitin ligase Nedd4-2 via enhanced channel ubiquitination. Here, we showed that SGK1 or SGK3 overexpression increased Nedd4-2 phosphorylation, which is known to inhibit Nedd4-2 activity. Nonetheless, disruption of the Nedd4-2 binding site in hERG channels did not eliminate the SGK-induced increase in hERG expression. Additional disruption of Rab11 proteins led to a complete elimination of SGK-mediated increase in hERG expression." According to the news reporters, the research concluded: "These results show that SGK enhances the expression level of mature hERG channels by inhibiting Nedd4-2 as well as by promoting Rab11-mediated hERG recycling." For more information on this research see: The serum- and glucocorticoid-inducible kinases SGK1 and SGK3 regulate hERG channel expression via ubiquitin ligase Nedd4-2 and GTPase Rab11. Journal of Biological Chemistry, 2013;288(21):15075-84. (American Society for Biochemistry and Molecular Biology - www.asbmb.org; Journal of Biological Chemistry - www.jbc.org/) Our news journalists report that additional information may be obtained by contacting S.M. Lamothe, Dept. of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada (see also Adrenal Cortex Hormones). Keywords for this news article include: Canada, Ontario, Ligases, Kingston, Proteins, Ubiquitins, Glucocorticoids, Enzymes and Coenzymes, Adrenal Cortex Hormones, North and Central America. Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC

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