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Validated All-in-One™ qPCR Primer for KCNK2(NM_001017425.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes one of the members of the two-pore-domain background potassium channel protein family. This type of potassium channel is formed by two homodimers that create a channel that leaks potassium out of the cell to control resting membrane potential. The channel can be opened, however, by certain anesthetics, membrane stretching, intracellular acidosis, and heat.
Gene References into function
- TREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein
- During hypoxia, modulation of hTREK1 cannot be accomplished by parameters known to be perturbed in brain ischemia. hTREK1 regulation in brain will be more relevant during alkalosis than during ischemia or acidosis.
- TREK-1 is inhibited by fluoxetine and norfluoxetine.
- hypoxic inhibition: (a) requires the C-terminal domain of the channel; (b) does not involve redox modulation of the C-terminal domain cysteine residues C365 and C399; and (c) is critically dependent on the glutamate residue at position 306
- receptor- and kinase-induced inhibition of TREK-1 background potassium channels is mediated by sequential phosphorylation
- human osteoblasts functionally express TREK-1 and that these channels contribute, at least in part, to the resting membrane potential of human osteoblast cells. We hypothesise a possible role for TREK-1 in mechanotransduction, leading to bone remodelling
- VOCCs and TREK channels have been implicated in mechanotransduction signaling pathways in numerous connective tissue cell types.
- TREK1, the most thoroughly studied K(2P) channel, has a key role in the cellular mechanisms of neuroprotection, anaesthesia, pain and depression--{REVIEW}
- These findings indicate that genetic variation in KCNK2 may identify individuals at risk for treatment resistance. More broadly, they indicate the utility of animal models in identifying genes for pharmacogenetic studies of antidepressant response.
- voltage-dependent C-type gating acceleration by protons represents a novel mechanism for K2P2.1 outward rectification.
- (Review) KCNK2, the gene encoding K2P2.1, can generate either full-length or K2P2.1D1-56 via alternative translation initiation, a mechanism which increases protein diversity by giving rise to two or more proteins from a single mRNA strand.
- Both TASK-3 and TREK-1 are functionally operational in the adrenocortical H295R cell line, modulate membrane potential and aldosterone secretion.