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Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. De plus, nous expédions KCNJ2 Protéines (5) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 121 products:
Mammalian Monoclonal KCNJ2 Primary Antibody pour ISt, IHC - ABIN1304735
DiFranco, Yu, Quiñonez, Vergara: Inward rectifier potassium currents in mammalian skeletal muscle fibres. dans The Journal of physiology 2015
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Dog (Canine) Polyclonal KCNJ2 Primary Antibody pour 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. dans Basic research in cardiology 2014
Human Polyclonal KCNJ2 Primary Antibody pour EIA, IHC (fro) - ABIN1107936
Hinard, Belin, Konig, Bader, Bernheim: Initiation of human myoblast differentiation via dephosphorylation of Kir2.1 K+ channels at tyrosine 242. dans Development (Cambridge, England) 2008
data show that hydrocinnamic acid can inhibit the currents of Kir2.1 channel in both excised inside-out and whole-cell patch with the IC50 of 5.21 +/- 1.02 and 10.08 +/- 0.46 mM, respectively.
study confirms the pathogenicity of Kir2.1-52V in 1 patient with long-QT syndrome and also supports the use of isogenic human induced pluripotent stem cell-derived cardiomyocytes as a physiologically relevant model for the screening of variants of unknown function.
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 (Montrer SCN5A Anticorps) N-terminal domain binding to alpha1-syntrophin (Montrer SNTA1 Anticorps) increases membrane density of human Kir2.1, Kir2.2 (Montrer KCNJ12 Anticorps) and Nav1.5 (Montrer SCN5A Anticorps) 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.
Following differentiation with LPS (Montrer TLR4 Anticorps) or a combination of LPS (Montrer TLR4 Anticorps) and IFN-gamma (Montrer IFNG Anticorps) microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa (Montrer CSN3 Anticorps) 3.1 and Kir (Montrer GEM Anticorps) currents, while microglia differentiated with IL-4 (Montrer IL4 Anticorps) exhibited large Kir (Montrer GEM Anticorps) 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa (Montrer CSN3 Anticorps) 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 (Montrer HIST1H4H Anticorps) hyperacetylation induced by Class I HDACs inhibitors promoted the expression profiles of potassium channels (Kcnj2, Kcnj3 (Montrer KCNJ3 Anticorps), Kcnj5 (Montrer KCNJ5 Anticorps), Kcnj11 (Montrer KCNJ11 Anticorps), and Kcnh2 (Montrer KCNH2 Anticorps))
Our results support the concept that endothelial cell Kir2 channels boost vasodilatory signals that are generated by Ca(2 (Montrer CA2 Anticorps)+) -dependent activation of IK and SK channels.
Results suggest that a promyogenic cell adhesion molecule (Montrer MCAM Anticorps) Cdo (Montrer CDO1 Anticorps) 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 (Montrer DMD Anticorps)-associated protein complex in the regulation of Kir2.x channels.
Intracellular Mg(2 (Montrer MCOLN1 Anticorps)+) and SPM (Montrer NPC1 Anticorps) therefore may have a synergistic action on the pore-blocking effect, presumably via prohibition of the outward exit of the higher-affinity blocking SPM (Montrer NPC1 Anticorps) by the lower-affinity Mg(2 (Montrer MCOLN1 Anticorps)+).
Hypoxic stress up-regulates Kir2.1 expression and facilitates cell proliferation in brain capillary endothelial cells.
Kir2.1 may mediate native Kir (Montrer GEM Anticorps) 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 (Montrer CACNA1C Anticorps), KChIP2 (Montrer KCNIP2 Anticorps), ERG (Montrer KCNH2 Anticorps), KvLQT1 (Montrer KCNQ1 Anticorps), Kir2.1, NCX1 (Montrer SLC8A1 Anticorps), SERCA2a (Montrer ATP2A2 Anticorps) and RyR2 (Montrer RYR2 Anticorps) 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