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KCNK1 encodes one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. Zusätzlich bieten wir Ihnen KCNK1 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal KCNK1 Primary Antibody für ICC, IF - ABIN4328480
Zhao, Xiong, Wilber, Cohen, Kreindler: A role for two-pore K⁺ channels in modulating Na⁺ absorption and Cl⁻ secretion in normal human bronchial epithelial cells. in American journal of physiology. Lung cellular and molecular physiology 2011
Dynamics of the TWIK-1 Channel
Our data indicate that TWIK-1 has a highly conserved role in cardiac function and is required for normal heart rate and atrial morphology. Despite the functional importance of TWIK-1 in the atrium, genetic variation in KCNK1 is not a common primary cause of human AF.
TWIK-1 protein possesses a hydrophobic barrier deep within the inner pore
Potassium channels, in particular K2P channels, are expressed and functional in the apical membrane of airway epithelial cells
study presents the 3.4 angstrom resolution crystal structure of a human K2P channel, K2P1; an extracellular cap domain located above the selectivity filter forms an ion pathway in which K(+) ions flow through side portals
ion selectivity of TWIK-1 K+ channels during pathological hypokalemia; a molecular basis for inward leak Na+ currents that could trigger or contribute to cardiac paradoxical depolarization in lowered [K+]o; mechanism for regulating cardiac excitability.
TWIK1 is internalized via a dynamin (zeige DNM1 Antikörper)-dependent mechanism and addressed to the recycling endosomal compartment. Mutation in its cytoplasmic C terminus (I293A,I294A) stabilizes TWIK1 at the plasma membrane, resulting in robust currents.
Removal of the peptide adduct by SUMO protease reveals K2P1 to be a K+-selective, pH-sensitive, openly rectifying channel regulated by reversible peptide linkage.
support TWIK-1 and TREK-1 (zeige KCNK2 Antikörper) as being the major components of the long-sought K(+) channels underlying the passive conductance of mature hippocampal astrocytes
the activation of mGluR3 (zeige GRM3 Antikörper) up-regulates the membrane expression of TWIK-1 that in turn enhances NH4(+) uptake in astrocytes.
KCNK1 was significantly induced during osteoclast differentiation, but its functional overexpression significantly inhibited osteoclast differentiation induced by RANKL (zeige TNFSF11 Antikörper)
TWIK-1 is functionally expressed in dentate gyrus granule cells and contributes to the intrinsic excitability of these cells.
TWIK-1/TREK-1 (zeige KCNK2 Antikörper) heterodimers mediate astrocytic passive conductance and cannabinoid-induced glutamate (zeige GRIN1 Antikörper) release from astrocytes.
A fall in quinidine-sensitive conductance could be an adaptive response in TWIK-1 knockout ducts.
This gene encodes one of the members of the superfamily of potassium channel proteins containing two pore-forming P domains. The product of this gene has not been shown to be a functional channel, however, it may require other non-pore-forming proteins for activity.
inward rectifying potassium channel protein TWIK-1
, potassium channel KCNO1
, potassium channel subfamily K member 1
, potassium inwardly-rectifying channel, subfamily K, member 1
, putative potassium channel TWIK
, potassium channel TWIK-1