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lack of Kir6.2 promoted neuronal differentiation via inhibiting the downregulation of glia cell line-derived neurotrophic factor (GDNF), which negatively related to the level of microRNA-133b.
reduced age-dependent weight gain of WNK1 TG mice seems to be related with the decreased Kir6.2 expression via WNK1- and WNK4-regulated protein stability of Kir6.2.
histone H4 hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2, Kcnj3, Kcnj5, Kcnj11, and Kcnh2)
both Kir6.1(V65M) and Kir6.2(V64M) mutations essentially abolish high-affinity sensitivity to the KATP blocker glibenclamide in both intact cells and excised patches. This raises the possibility that, at least for some CS mutations, sulfonylurea therapy may not prove to be successful and highlights the need for detailed pharmacogenomic analyses of CS mutations.
data demonstrate that increased Kir6.2 is seen in reactive astrocytes in old 3xTg-Alzheimer's disease (AD) mice and human AD tissue
ATP-sensitive K(+) Kir6.2 channels may play a novel role in regulating myocardial energy metabolism.
Cardiac ischemia causes a loss of the sarcolemmal KATP channel density by internalization through a pathway mediated by dynamin-dependent endocytosis and CaMKII-mediated signaling. Ischemic preconditioning counteracts thiscloss and restores the density of the sarcolemmal KATP channels.
Lack of kcnj11 expression increases peroxynitrite-mediated modification of the key calcium-handling protein sarcoendoplasmic reticulum Ca(2+)-ATPase after myocardial ischemia-reperfusion injury, contributing to impaired diastolic function.
K(ATP) channels seem to play an essential role in murine myometrial motility via activation of SUR2B and Kir6.2
A Conserved Residue Cluster That Governs Kinetics of ATP-dependent Gating of Kir6.2 Potassium Channels.
ATP-sensitive potassium currents from channels formed by Kir6 and a modified cardiac mitochondrial SUR2 variant
The Kir6.2-containing K-ATP channel is required for cardioprotection of resveratrol.
Report mechanical dyssynchrony as an early marker of cardiomyopathic disease in ATP-sensitive K channel-deficient dilated cardiomyopathy.
a role of K(ATP)-channel-dependent neuronal excitability in catecholaminergic neurons in maintaining thermogenic BAT sympathetic tone and energy homeostasis.
Data indicate that betaIV-Spectrin-targeted CaMKII directly phosphorylates the inwardly-rectifying potassium channel, Kir6.2.
Kir6.2 subunits are critical in resistance to endotoxemia-induced cardiac dysfunction through reducing myocardial damage by inhibition of apoptosis and inflammation.
These findings reveal unrecognized slide helix elements that are required for functional channel expression and control of Kir6.2 gating by intracellular ATP.
We found that perfused hearts from Kir6.2(-/-) mice exhibited a normal baseline response to ischemia-reperfusion injury, were not protected by ischemic preconditioning
Data from Kir6.2 knockout mice suggest that KATP channel-independent mechanism mediated by vagus nerve plays critical role in insulin secretion by pancreatic beta cells in response to eating of dietary carbohydrates.
CaMKII phosphorylation of Kir6.2 promotes endocytosis of cardiac ATP-sensitive potassium channels.
The study is the first report of a novel form of late-onset persistent hyperinsulinemic hypoglycemia of infancy (PHHI) that is caused by a dominant mutation in KCNJ11 and exhibits a defect in proper surface expression of Kir6.2.
Genetic variation in the KCNJ11 is associated with Prediabetes.
A lasso extension forms an interface between SUR1 and Kir6.2 adjacent to the ATP site in the propeller form and is disrupted in the quatrefoil form. These structures support the role of SUR1 as an ADP sensor and highlight the lasso extension as a key regulatory element in ADP's ability to override ATP inhibition.
Combination of heterozygous mutations in the ABCC8 and KCNJ11 genes could also lead to beta cells dysfunction presenting as congenital hyperinsulinism.
It was confirmed that this deletion in the KCNJ11 gene did not affect the protein expression levels of key pluripotent factors. Additionally, normal karyotype and differentiation potency were observed for the cell line.
Genetic variants in KCNJ11 gene had significantly decreased pancreas weight and insulin mass similar to that of type 1 diabetes.
genetic association studies in pediatric population in Japan: Data confirm that mutations in KCNJ11 or ABCC8 are associated with neonatal diabetes mellitus. Novel mutations were identified; 2 in KCNJ11 (V64M, R201G) and 6 in ABCC8 (R216C, G832C, F1176L, A1263V, I196N, T229N). (KCNJ11 = ATP-sensitive inward rectifier potassium channel-11; ABCC8 = ATP-binding cassette subfamily C member-8)
Data suggest that patients with NDM (permanent neonatal diabetes mellitus) related to mutations in KCNJ11 are at increased risk for delays in learning, delays in social-emotional-behavioral development, sleep difficulties, and ADHD (attention deficit hyperactivity disorder) based on parent/guardian reports.
When typing at the polymorphic loci in the Glu23Lys in the KCNJ11 gene, the development of type 2 Diabetes Mellitus in the Kyrgyz population was associated with the T allele the 23Lys allele (OR, 1.62; p=0.019) in the KCNJ11 gene.
Evaluation of Glutathione Peroxidase and KCNJ11 Gene Polymorphisms in Patients with New Onset Diabetes Mellitus After Renal Transplantation.
Herein, we report the clinical features of two siblings with a heterozygous mutation C679 G>A in the KCNJ11 gene.
Upregulated KCNJ11 predicts a poor prognosis and is regulated by NFkappaB signaling in hepatocellular carcinoma (HCC). LDHA partially mediated the oncogenic roles of KCNJ11 in HCC.
Description of the variety of neurodevelopmental problems seen in those with KCNJ11 mutations, even in those without recognized global developmental delays.
Systematic assessment using standardized validated questionnaires reveals a range of psychiatric morbidity in children with KCNJ11 neonatal diabetes. This is under-recognized clinically and has a significant impact on affected children and their families. An integrated collaborative approach to clinical care is needed to manage the complex needs of people with KCNJ11 neonatal diabetes.
KCNJ11 mutation causing loss of function of beta-cell KATP channels lead to congenital hyperinsulinism, higher basal [Ca(2+)] i and insulin secretion, increased insulin secretion in response to amino acids but not to glucose, increased basal rate of oxygen consumption and mitochondrial mass, increased rates of glycolysis, increased serine/glycine and glutamine biosynthesis, and low gamma-aminobutyric acid (GABA) levels.
Functional studies indicated that the Kir6.2-G324R mutation reduces the channel ATP sensitivity but that the difference in ATP inhibition between homozygous and heterozygous channels is remarkably small. Nevertheless, the homozygous patient developed neonatal diabetes, whereas the heterozygous parents were, and remain, unaffected.
KCNJ11 expression is decreased in human ischemia cardiomyopathy.
KCNJ11 mutation is associated with permanent neonatal diabetes mellitus.
The polymorphic marker Glu23Lys in the KCNJ11 gene is associated with hypertension in Kyrgyzia.
Although the expression level of Kir6.2 channel subtype does not differ between aortic smooth muscle cells of control and hypertrophied models, those of Kir6.1 and SUR2B subtypes are reduced in left ventricular hypertrophy models.
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1), inward rectifying potassium channel (Kir6.2, associated with Sur1), glucagon-like peptide 1 receptor (GLP1R), and adrenergic receptor alpha 2A (ADRalpha2A)
The predominant K(ATP) channel expressed in pig urethral smooth muscle possesses a unique, heteromeric pore structure with a pore-forming subunit composition of (Kir6.1)(3)-(Kir6.2).
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 and is found associated with the sulfonylurea receptor SUR. Mutations in this gene are a cause of familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion. Defects in this gene may also contribute to autosomal dominant non-insulin-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM). Multiple alternatively spliced transcript variants that encode different protein isoforms have been described for this gene.
potassium inwardly-rectifying channel, subfamily J, member 11
, potassium inwardly-rectifying channel J11
, ATP-sensitive inward rectifier potassium channel 11
, ATP-sensitive inward rectifier potassium channel 11-like
, inward rectifier K(+) channel Kir6.2
, potassium channel, inwardly rectifying subfamily J member 11
, potassium inwardly-rectifying channel subfamily J member 11
, inward rectifier potassium channel Kir6.2
, beta-cell inward rectifier subunit
, inwardly rectifying potassium channel KIR6.2
, potassium channel inwardly rectifing subfamily J member 11
, potassium inwardly rectifying channel, subfamily J, member 11
, ATP-sensitive inward rectifier potassium channel Kir6.2
, inwardly rectifying potassium channel Kir6.2