Lane 1: Human placenta
Lane 2: Human liver
Rabbit polyclonal primary
KCNK1 Rabbit Polyclonal Antibody (ER1803-39)
Synthetic peptide within human kcnk1 aa 40-100.
Human placenta tissue, human liver tissue, rat cerebellum tissue, human kidney tissue, mouse brain tissue, SH-SY-5Y.
Store at +4C after thawing. Aliquot store at -20C. Avoid repeated freeze / thaw cycles.
1*PBS (pH7.4), 0.2% BSA, 50% Glycerol. Preservative: 0.05% Sodium Azide.
Peptide affinity purified.
DPK antibody; HOHO antibody; HOHO1 antibody; inward rectifying potassium channel protein TWIK 1 antibody; Inward rectifying potassium channel protein TWIK-1 antibody; Inward rectifying potassium channel protein TWIK1 antibody; K2P1 antibody; K2p1.1 antibody; KCNK1 antibody; KCNK1_HUMAN antibody; KCNO1 antibody; OTTHUMP00000036029 antibody; Potassium channel KCNO1 antibody; Potassium channel subfamily K member 1 antibody; Potassium inwardly rectifying channel subfamily K member 1 antibody; TWIK 1 antibody; TWIK1 antibody
Belongs to the two pore domain potassium channel (TC 1.A.1.8) family.
Detected in bronchial epithelial cells. Detected in heart left atrium and left ventricle. Detected in cardiac myocytes (at protein level). Widely expressed with high levels in heart, brain and kidney, and lower levels in colon, ovary, placenta, lung and liver. Highly expressed in cerebellum, and detected at lower levels in amygdala, caudate nucleus, brain cortex, hippocampus, putamen, substantia nigra, thalamus, dorsal root ganglion, spinal cord, pituitary, heart, kidney, lung, placenta, pancreas, stomach, small intestine, uterus and prostate. Detected in right and left heart ventricle and atrium, and in heart Purkinje fibers. Detected in bronchial epithelial cells.
Sumoylation is controversial. Sumoylated by UBE2I. Not sumoylated when expressed in xenopus oocytes or mammalian cells. Sumoylation inactivates the channel, but does not interfere with expression at the cell membrane. Sumoylation of a single subunit is sufficient to silence the dimeric channel. Sumoylation of KCNK1 is sufficient to silence heterodimeric channels formed by KCNK1 and KCNK3 or KCNK9. Desumoylated by SENP1; this activates the channel. Desumoylated by SENP1; this strongly increases halothane-mediated activation of heterodimeric channels formed with KCNK9. SENP1 treatment has no effect.
Cell junction. Cell membrane. Cell projection. Cytoplasmic vesicle. Endosome. Membrane. Synapse.
Ion channel that contributes to passive transmembrane potassium transport and to the regulation of the resting membrane potential in brain astrocytes, but also in kidney and in other tissues. Forms dimeric channels through which potassium ions pass in accordance with their electrochemical gradient. The channel is selective for K+ ions at physiological potassium concentrations and at neutral pH, but becomes permeable to Na+ at subphysiological K+ levels and upon acidification of the extracellular medium. Channel activity is modulated by activation of serotonin receptors. Heterodimeric channels containing KCNK1 and KCNK2 have much higher activity, and may represent the predominant form in astrocytes. Heterodimeric channels containing KCNK1 and KCNK3 or KCNK9 have much higher activity. Heterodimeric channels formed by KCNK1 and KCNK9 may contribute to halothane-sensitive currents. Mediates outward rectifying potassium currents in dentate gyrus granule cells and contributes to the regulation of their resting membrane potential. Contributes to the regulation of action potential firing in dentate gyrus granule cells and down-regulates their intrinsic excitability. In astrocytes, the heterodimer formed by KCNK1 and KCNK2 is required for rapid glutamate release in response to activation of G-protein coupled receptors, such as F2R and CNR1.