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both Kir6.1 (zeige KCNJ8 Proteine)(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 (zeige DNM1 Proteine)-dependent endocytosis and CaMKII (zeige CAMK2G Proteine)-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 (zeige ABCC9 Proteine) 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 (zeige ABCC9 Proteine) 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 (zeige KCNC4 Proteine)-deficient dilated cardiomyopathy.
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.
Cross-linking experiments showed that KATP channel inhibitors promoted interactions between the N terminus of Kir6.2 and SUR1, whereas channel openers did not, suggesting the inhibitors enhance intersubunit interactions to overcome channel biogenesis and trafficking defects.
The genotype (EE/EK/KK) frequencies (%) for the CTRL group (38.2/50.2/11.6), Type 1 Diabetes (34.3/52.0/13.7), and Type 2 Diabetes (38.2/48.9/12.9) were in Hardy-Weinberg equilibrium and there were no significant differences. The minor allele frequencies (MAF; K) for CTRL (37.0%), Type 1 Diabetes (39.7%), and Type 2 Diabetes (37.4%) were not different among the groups
KCNJ11 mutation is associated with permanent neonatal diabetes.
A male infant who was diagnosed with congenital hyperinsulinism (CHI) with a novel homozygous p.F315I mutation in the kcnj11 channel (KCNJ11) gene, and parents were second cousins both with heterozygous mutations for this gene, and the patient was successfully managed with sirolimus therapy.
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 (zeige KCNJ8 Proteine) and SUR2B (zeige ABCC9 Proteine) subtypes are reduced in left ventricular hypertrophy models.
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1 (zeige ABCC8 Proteine)), inward rectifying potassium channel (zeige KCNAB2 Proteine) (Kir6.2, associated with Sur1 (zeige ABCC8 Proteine)), glucagon-like peptide 1 receptor (GLP1R (zeige GLP1R Proteine)), and adrenergic receptor alpha 2A (zeige ADRA2A Proteine) (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 (zeige KCNJ8 Proteine))(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