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Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. Additionally we are shipping KCNJ8 Antibodies (85) and many more products for this protein.
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KCNJ8-S422L as pathogenic for J-wave syndromes failed to appropriately account for European population structure and the variant is likely benign, or (b) Ashkenazi Jews may be at significantly increased risk of J-wave syndromes
We identified a de novo missense mutation encoding Kir6.1[p.Cys176Ser] in the patient. Kir6.1[p.Cys176Ser] channels exhibited markedly higher activity than wild-type channels, as a result of reduced ATP sensitivity.
Data indicate that pharmacological KvLQT1 (show KCNQ1 Proteins) and KATP (Kir6.1) inhibition or silencing with siRNAs down-regulated alpha-ENaC (show SCNN1A Proteins) expression.
The KCNJ8-S422L variant was shown to be associated with both increased susceptibility to atrial fibrillation and early repolarization.
results suggest that acting on the 3'-UTR of Kir6.1 and the coding region of SUR2B (show ABCC9 Proteins), methylglyoxal causes instability of Kir6.1 and SUR2B (show ABCC9 Proteins) mRNAs, disruption of vascular K(ATP) channels, and impairment of arterial function
Data suggest that Kir6.1 and M3 muscarinic receptor (show CHRM3 Proteins) colocalize to detrusor caveolae; studies include tissue from both male and female subjects.
The researchers report evidence that the KCNJ8 gene increases susceptiblity to the brugada syndrome and early repolarization syndrome.
The mutations localized to Kir6.1's C-terminus, involved conserved residues and the pinacidil-activated K(ATP) current was decreased 45% to 68% for Kir6.1-E332del and 40% to 57% for V346I between -20 mV and 40 mV.
Down-regulation of Kir6.1 and Kir6.2 (show KCNJ11 Proteins) expression in myometrium may contribute to the enhanced uterine contractility associated with the onset of labour.
Interaction with caveolin-1 causes a shift the channel's sensitivity to its physiological regulator magnesium ADP (MgADP).
Similar to previous results in Kir6.1(-/-) myocytes, Kir6.1 gain of function myocytes demonstrate resistance (less volume derangement) to stress of cardioplegia.
K(ATP) channel gain-of-function leads to increased myocardial L-type Ca(2 (show CA2 Proteins)+) current and contractility in Cantu (show ABCC9 Proteins) syndrome.
Kcnj8 mutation is responsible of heart conduction abnormalities in Cantu (show ABCC9 Proteins) syndrome.
our study demonstrated that exercise training up-regulated Kir6.1, improved tissue oxygenation recovery, and protected the heart against I/R injury
Results suggest that the vascular KATP channel Kcnj8 is organ protective in diabetic conditions.
The absence of Kir6.1 does not affect the contractile properties of myocytes during stress, suggesting the absence of Kir6.1 improves myocyte tolerance to stress via an unknown mechanism.
Sulfhydration of SUR2B (show ABCC9 Proteins) subunit modifies tyrosine nitration of Kir6.1 subunit within the KATP channel complex.
Kir6.1 underlies the vascular smooth muscle KATP channel and has a key role in vascular reactivity and blood pressure control.
Native K(ATP) channels in mouse vas (show AVP Proteins) deferens myocytes are a heterocomplex of K(IR)6.1 channels and SUR2B (show ABCC9 Proteins) subunits.
Kir6.1 knockdown exacerbates cerebral ischemia reperfusion-induced brain damage.
Results describe a new function of the Kir6.1-SUR2A (show ABCC9 Proteins) complex, namely the regulation of paracellular permeability through tight junctions.
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 (show KCNJ11 Proteins)).
Kir6.1/SUR2B is the major functional K(ATP) channel complex in the pig MMA and MCA, and mRNA expression studies suggest that the human MMA shares this K(ATP) channel subunit profile
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. Defects in this gene may be a cause of J-wave syndromes and sudden infant death syndrome (SIDS).
potassium inwardly-rectifying channel, subfamily J, member 8
, Kir 6.1
, potassium inwardly-rectifying channel J8
, ATP-sensitive inward rectifier potassium channel 8
, inward rectifier K(+) channel Kir6.1
, inwardly rectifying potassium channel KIR6.1
, potassium channel, inwardly rectifying subfamily J member 8
, inwardly rectifier K(+) channel Kir6.1
, Inwardly rectifying potassium channel gene subfamily J-8 (ATP sensitive)
, Inwardly rectifying potassium channel gene, subfamily J-8 (ATP sensitive)
, Kir6.1 like