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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 (zeige ENPEP Proteine) 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 (zeige ENPEP Proteine) carrying the 2 most common KCNJ5 somatic mutations.
KCNJ5(T158A)increases CYP11B2 (zeige CYP11B2 Proteine) 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 (zeige POMC Proteine) 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 (zeige GRIK4 Proteine) 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 (zeige KCNJ3 Proteine)/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 (zeige KCNJ3 Proteine) subunit functions like a GIRK4 subunit with Na+ permanently bound.
These results provide a novel molecular mechanism for autocrine negative feedback regulation of insulin (zeige INS Proteine) 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
Data indicate taht m2R-RGS6 (zeige RGS6 Proteine)-IKACh pathway sets heart rate variability independently from the autonomic input.
Therefore, the lack of proper functioning of the cardio-protective K(ATP) system in the mdx (zeige DMD Proteine) cardiomyocytes may be part of the mechanism contributing to development of cardiac disease in dystrophic patients.
Data suggest HL-1 (zeige ASGR1 Proteine) cells express GIRK1 (zeige KCNJ3 Proteine)/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 (zeige KCNJ3 Proteine) and Kir (zeige GEM Proteine) 3.4 subunits of the G protein-gated potassium channel (zeige KCNAB2 Proteine) changes during embryonic development.
These data implicate GIRK4-containing channels in signaling crucial to energy homeostasis and body weight.
Blockade of K(ATP) channels further diminished (approximately 45%) the repayment of flow debt (zeige PLXNB2 Proteine) 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