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Research Letter: KCNJ5 mutation (145 - 147delETEinsK) detected in a female patient with aldosterone-producing adenoma.
Testing for KCNJ5 mutations in young patients with aldosterone-producing adenoma may provide a prognostic indication for resolution of hypertension and severity of vascular complications.
Next-generation sequencing of DNA from Idiopathic Hyperaldosteronism Aldosterone-producing cell cluster demonstrated somatic mutations in genes encoding the KCNJ5.
Potassium inwardly-rectifying channel subfamily J member 5 (KCNJ5)-mutated aldosterone-producing adenomas (APAs) had significantly more abundant and smaller-sized mitochondria with well-developed cristae than wild type, whereas wild type had more abundant lipid droplets.
Macrolides for KCNJ5-mutated aldosterone-producing adenoma (MAPA): design of a study for personalized diagnosis of primary aldosteronism.
Recurrent KCNJ5 mutations have subsequently been demonstrated in large series of Aldosterone-producing Adenomas worldwide.
germline mutations cause familial hyperaldosteronism type III [revew]
DNA hypomethylation and gene expression changes in Wnt signaling and inflammatory response pathways were characteristic of APAs with KCNJ5 mutations.
rs2604204 polymorphism related to increased plasma aldosterone level, but also plasma renin, angiotensin I and II levels in newly diagnosed, never-treated hypertension patients
our results provide evidence that during 12 months of follow-up of APA patients after adrenalectomy, KCNJ5 mutational status was not associated with the improvement of arterial stiffness. Clinically, patients who are younger tend to have an advantage in being cured of hypertension after adrenalectomy.
An aldosterone-driving KCNJ5 mutation was detected in juvenile primary aldosteronism, but not in the histologically normal cortex.
By proving the principle that the oversecretion of aldosterone can be specifically blunted in APA cells ex vivo with G151R and L168R mutations, these results provide compelling evidence of the possibility of specifically correcting aldosterone excess in patients with APA carrying the 2 most common KCNJ5 somatic mutations.
KCNJ5(T158A)increases CYP11B2 expression and production of aldosterone, corticosterone and hybrid steroids by upregulating both acute and chronic regulatory events in aldosterone production, and verapamil blocks KCNJ5(T158A)-mediated pathways leading to aldosterone production.
These findings expand on the clinical spectrum of phenotypes associated with KCNJ5 mutations and implicate these mutations in the pathogenesis of hypertension associated with increased aldosterone response to ACTH stimulation.
KCNJ5 mutations predominate in large zona fasciculata (ZF)-like Aldosterone-producing Adenomas.
Mutations in KCNJ5 cause the excessive autonomous aldosterone secretion of Aldosterone-producing Adenomas.
KCNJ5 genetic mutation plays a role in the development of primary aldosteronism in aldosterone producing adenomas.
Study provides new evidence, indicating that some glutamate receptor ionotropic kainate 4 variants modulate the response to electroconvulsive therapy in patients with depression resistant to treatment, suggesting a role for kainate receptor modulation.
documented for the first time the expression of inflammation-related genes in aldosterone-producing adenomas (APAs) and the correlation of their expression levels with the KCNJ5 mutation status and mRNA expression levels of steroidogenic enzymes, indicating the pathophysiological relevance of inflammation-related genes in APAs
GIRK1/GIRK4 hetero-tetramers are not activated by Na+, but rather are in a permanent state of high responsiveness to G proteins beta-gamma, suggesting that the GIRK1 subunit functions like a GIRK4 subunit with Na+ permanently bound.
Data show that potassium inwardly-rectifying channel subfamily J member 5 (Kcnj5) is important for baseline aldosterone secretion, but its importance is sex-limited at least in the mouse.
histone H4 hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2, Kcnj3, Kcnj5, Kcnj11, and Kcnh2)
These results provide a novel molecular mechanism for autocrine negative feedback regulation of insulin secretion.
study establishes the role of f-channels in cardiac automaticity and indicates that arrhythmia related to HCN loss-of-function may be managed by pharmacological or genetic inhibition of GIRK4 channels
expressed in outer sarcolemmas and ventricular t-tubular system of mouse heart
Data indicate taht m2R-RGS6-IKACh pathway sets heart rate variability independently from the autonomic input.
the K(ATP) channel may have an important physiological role during early cardiac development.
Therefore, the lack of proper functioning of the cardio-protective K(ATP) system in the mdx cardiomyocytes may be part of the mechanism contributing to development of cardiac disease in dystrophic patients.
Our present study reinforces a role for the sulfonylurea-sensitive KATP channel in cardioprotection.
Data suggest HL-1 cells express GIRK1/4 and M2 muscarinic receptors and are a good model to study acetylcholine-activated potassium currents.
Data show that the composition of the Kir3.1 and Kir 3.4 subunits of the G protein-gated potassium channel changes during embryonic development.
Girk exhibite in Golgi cells of cerebellum.
These data implicate GIRK4-containing channels in signaling crucial to energy homeostasis and body weight.
These results suggested that morphine-induced delayed PC has a protective effect during A/R injury of PAECs. This effect may be mediated by mitochondrial KATP channels and is opioid receptor-dependent.
Blockade of K(ATP) channels further diminished (approximately 45%) the repayment of flow debt in lean but not metabolic syndrome swine.
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins. It may associate with two other G-protein-activated potassium channels to form a heteromultimeric pore-forming complex.
G protein-activated inward rectifier potassium channel 4
, cardiac ATP-sensitive potassium channel
, heart KATP channel
, inward rectifier K+ channel KIR3.4
, cardiac inward rectifier
, inward rectifier K(+) channel Kir3.4
, potassium channel, inwardly rectifying subfamily J member 5
, inward rectifying K channel
, potassium inwardly-rectifying channel J5
, Cardiac inward rectifier
, Heart KATP channel
, Inward rectifier K(+) channel Kir3.4
, Potassium channel, inwardly rectifying subfamily J member 5
, potassium inwardly-rectifying channel, subfamily J, member 5