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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 KCNJ2 Proteins (5) and many more products for this protein.
Showing 10 out of 94 products:
Mammalian Monoclonal KCNJ2 Primary Antibody for ISt, IHC - ABIN1304735
DiFranco, Yu, Quiñonez, Vergara: Inward rectifier potassium currents in mammalian skeletal muscle fibres. in The Journal of physiology 2015
Show all 9 Pubmed References
Human Polyclonal KCNJ2 Primary Antibody for EIA, IHC (fro) - ABIN1107936
Hinard, Belin, Konig, Bader, Bernheim: Initiation of human myoblast differentiation via dephosphorylation of Kir2.1 K+ channels at tyrosine 242. in Development (Cambridge, England) 2008
Dog (Canine) Polyclonal KCNJ2 Primary Antibody for WB - ABIN2177159
Zhao, Xu, Yun, Zhao, Li, Gong, Yuan, Yan, Zhang, Ding, Wang, Zhang, Dong, Xiu, Yang, Liu, Xue, Li: Chronic obstructive sleep apnea causes atrial remodeling in canines: mechanisms and implications. in Basic research in cardiology 2014
We report a novel KCNJ2 sequence variant (p.Y145C) in a family with diagnosed Andersen-Tawil syndrome.
Combined inhibition of IKr and IKur produced a synergistic anti-arrhythmic effect in both forms of SQT3. In conclusion, this study provides mechanistic insights into atrial proarrhythmia with SQT3 Kir2.1 mutations and highlights possible pharmacological strategies for management of SQT3-linked AF.
Data suggest that an R204A mutation disrupts the characteristic cytoplasmic domain subunit interface salt bridges in Kir2.1 reducing apparent sensitivity of channel activity to ligand PIP2 (phosphatidylinositol bisphosphate).
These findings suggest that KCNJ2 plays an important role in the pathophysiology of Thyrotoxic Periodic Paralysis in Korean Graves' Disease patients with Thyrotoxic Periodic Paralysis .
Nav1.5 (show SCN5A Antibodies) N-terminal domain binding to alpha1-syntrophin (show SNTA1 Antibodies) increases membrane density of human Kir2.1, Kir2.2 (show KCNJ12 Antibodies) and Nav1.5 (show SCN5A Antibodies) channels
Kir2.1 may participate in macrophage maturation and differentiation, and play a key role in lipid uptake and foam cell formation through modulating the expression of scavenger receptors.
a Korean family with Andersen-Tawil syndrome with a G215D mutation of the KCNJ2 gene revealed by diagnostic exome sequencing, is reported.
Chloroethylclonidine interact with Kir2.1 channels in the cytoplasmic pore.
Variability has been found in a three-generation family with Pierre Robin sequence, acampomelic campomelic dysplasia, and intellectual disability due to a novel approximately 1 Mb deletion upstream of SOX9 (show SOX9 Antibodies), and including KCNJ2 and KCNJ16 (show KCNJ16 Antibodies).
Patients with Dilated Cardiomyopathy and Sustained Monomorphic Ventricular Tachycardia Show Up-Regulation of KCNN3 (show KCNN3 Antibodies) and KCNJ2 Genes and CACNG8 (show CACNG8 Antibodies)-Linked Left Ventricular Dysfunction
Following differentiation with LPS (show TLR4 Antibodies) or a combination of LPS (show TLR4 Antibodies) and IFN-gamma (show IFNG Antibodies) microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa (show CSN3 Antibodies) 3.1 and Kir (show GEM Antibodies) currents, while microglia differentiated with IL-4 (show IL4 Antibodies) exhibited large Kir (show GEM Antibodies) 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa (show CSN3 Antibodies) 3.1 currents were generally low
Cellular electrophysiology assays of mouse Kir2.1 and human Kir2.2 indicated that, consistent with simulations, the Leu residue increased the channel responses to phosphatidylinositol diphosphate (PIP2) through increased binding affinity and faster activation kinetics, and the deactivation kinetics decreased upon PIP2 inhibition.
histone H4 (show HIST1H4H Antibodies) hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2, Kcnj3 (show KCNJ3 Antibodies), Kcnj5 (show KCNJ5 Antibodies), Kcnj11 (show KCNJ11 Antibodies), and Kcnh2 (show KCNH2 Antibodies))
Our results support the concept that endothelial cell Kir2 channels boost vasodilatory signals that are generated by Ca(2 (show CA2 Antibodies)+) -dependent activation of IK and SK channels.
Results suggest that a promyogenic cell adhesion molecule (show MCAM Antibodies) Cdo (show CDO1 Antibodies) signaling is critical for Inward rectifier potassium channel Kir2.1 activities in the induction of myogenic differentiation.
The data suggest that microglial Kir2.1 channels may represent novel therapeutic targets to inhibit excessive reactive oxygen species production by primed microglia in brain pathology.
Three pairs of weak interactions precisely regulate the G-loop gate of Kir2.1 channel.
Suggest that Kir2.1 channels, in part, account for hyperpolarization and associated absence of tone in urinary bladder arterioles.
This finding represents the first functional evidence for a significant role of the dystrophin (show DMD Antibodies)-associated protein complex in the regulation of Kir2.x channels.
Intracellular Mg(2 (show MCOLN1 Antibodies)+) and SPM (show NPC1 Antibodies) therefore may have a synergistic action on the pore-blocking effect, presumably via prohibition of the outward exit of the higher-affinity blocking SPM (show NPC1 Antibodies) by the lower-affinity Mg(2 (show MCOLN1 Antibodies)+).
Hypoxic stress up-regulates Kir2.1 expression and facilitates cell proliferation in brain capillary endothelial cells.
Kir2.1 may mediate native Kir (show GEM Antibodies) currents responsible for setting resting membrane potential in bovine parotid cells and might be, at least in part, involved in spontaneous secretion in ruminant parotid glands.
There were substantial transmural gradients in Cav1.2 (show CACNA1C Antibodies), KChIP2 (show KCNIP2 Antibodies), ERG (show KCNH2 Antibodies), KvLQT1 (show KCNQ1 Antibodies), Kir2.1, NCX1 (show SLC8A1 Antibodies), SERCA2a (show ATP2A2 Antibodies) and RyR2 (show RYR2 Antibodies) at the mRNA and, in some cases, protein level-in every case the mRNA or protein was more abundant in the epicardium than the endocardium.
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, probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Mutations in this gene have been associated with Andersen syndrome, which is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features.
, inward rectifier K(+) channel Kir2.1
, inward rectifier potassium channel 2
, potassium channel, inwardly rectifying subfamily J member 2
, cardiac inward rectifier potassium channel
, inward rectifier K+ channel KIR2.1
, inward rectifier potassium channel cIRK1
, cardiac inward rectifier KIR2.1
, inwardly rectifying potassium channel Kir2.1
, inward rectifier potassium channel Kir2.1
, inwardly-rectifying potassium channel Kir2.1