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reduced age-dependent weight gain of WNK1 (show WNK1 Proteins) TG mice seems to be related with the decreased Kir6.2 expression via WNK1 (show WNK1 Proteins)- and WNK4 (show WNK4 Proteins)-regulated protein stability of Kir6.2.
histone H4 hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2 (show KCNJ2 Proteins), Kcnj3 (show KCNJ3 Proteins), Kcnj5 (show KCNJ5 Proteins), Kcnj11, and Kcnh2 (show KCNH2 Proteins))
both Kir6.1 (show KCNJ8 Proteins)(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 (show DNM1 Proteins)-dependent endocytosis and CaMKII (show CAMK2G Proteins)-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 (show ABCC9 Proteins) 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 (show ABCC9 Proteins) variant
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 (show ABCC8 Proteins) 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 (show INS Proteins) 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 (show GPX1 Proteins) and KCNJ11 Gene Polymorphisms in Patients with New Onset Diabetes Mellitus After Renal Transplantation.
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 (show KCNJ8 Proteins) and SUR2B (show ABCC9 Proteins) subtypes are reduced in left ventricular hypertrophy models.
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1 (show ABCC8 Proteins)), inward rectifying potassium channel (show KCNAB2 Proteins) (Kir6.2, associated with Sur1 (show ABCC8 Proteins)), glucagon-like peptide 1 receptor (GLP1R (show GLP1R Proteins)), and adrenergic receptor alpha 2A (show ADRA2A Proteins) (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 (show KCNJ8 Proteins))(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