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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 Potassium Inwardly-Rectifying Channel, Subfamily J, Member 6 Antibodies (72) and many more products for this protein.
Showing 7 out of 7 products:
The KCNJ6 -1250A and COMT (show COMT Proteins) Val alleles are predisposing preterm newborns to diminished opioid-induced pain relief.
The major findings of the current study are 1) an additive genotypic effect of the KCNJ6 SNP on the ERO theta power phenotype during reward processing, increasing significantly across genotypes.
Three of the four KCNJ6 SNPs studied here were found to be significantly associated with the same theta event related oscillations in adults.
The findings of this study suggest that variations in KCNJ6 genes are associated with both mild and severe persistent breast pain after breast cancer surgery.
KCNJ6 (GIRK2) gene polymorphism rs2835859 could serve as a marker that predicts sensitivity to analgesics and pain and susceptibility to nicotine dependence.
In this transgenic mouse model, GIRK2 plays a major role in the genesis of infantile spasms.
Keppen-Lubinsky syndrome is caused by mutations in the inwardly rectifying K+ channel (show KCNJ1 Proteins) encoded by KCNJ6.
For KCNJ6, three SNPs (i.e., rs2835914, rs8129919, rs2836050) were associated with the occurrence of preoperative breast pain.
Ethanol associates directly with the GIRK channel, leading to enhanced interaction with a membrane phospholipid phosphatidylinositol 4,5-bisphosphate and activation of the channel.
3.5 A resolution crystal structure of the mammalian GIRK2 channel in complex with betagamma G-protein subunits, the central signalling complex that links G-protein-coupled receptor (show ADRA1A Proteins) stimulation to K(+) channel (show KCNC4 Proteins) activity
Results indicate that the properties and inhibitory activity of dorsal raphe neurons are highly regulated by G protein-coupled inwardly rectifying K+ (GIRK) 2 subunit-containing channels, introducing GIRK channels as potential candidates for studying the pathophysiology and treatment of affective disorders.
Increased Kcnj6 gene dose is necessary for synaptic and cognitive dysfunction in the animal model of Down Syndrome.
The GABABR-coupled GIRK2 channel is necessary for the GABABR agonist-induced infantile spasms phenotype in the Ts mouse and may represent a novel therapeutic target for the treatment of infantile spasms in Down syndrome.
It was concluded that GIRK2, through its dual responsiveness to G protein beta (show GNB3 Proteins)-gamma and Na+, mediates a form of neuronal inhibition that is amplifiable in the setting of excess electrical activity.
cholesterol did not affect the unitary conductance of GIRK2, it significantly enhanced the frequency of channel openings.
Results indicate that GIRK channels formed by GIRK2 subunits determine depression-related behaviors as well as basal and 5-HT1A receptor (show CC2D1A Proteins)-mediated dorsal raphe neuronal activity
This study showed that spontaneous GIRK2 mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
This study demonstrated that the residue Ser-196 in Kir3.2 is involved in conferring PKC-mediated inhibition to the channel.
In the ventral tegmental area, GABA neurons express both GIRK2 (and GIRK1 (show KCNJ3 Proteins)) subunits.
Gbeta (show SUCLG2 Proteins)-gamma and PIP2 must be present simultaneously to activate GIRK2.
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, is controlled by G-proteins and may be involved in the regulation of insulin secretion by glucose. It associates with two other G-protein-activated potassium channels to form a heteromultimeric pore-forming complex.
potassium inwardly-rectifying channel, subfamily J, member 6
, G-protein-coupled inward rectifier potassium channel
, G protein-activated inward rectifier potassium channel 2
, inward rectifier K(+) channel Kir3.2
, inward rectifier potassium channel KIR3.2
, potassium channel, inwardly rectifying subfamily J member 6
, potassium inwardly-rectifying channel J6
, Inward rectifier K(+) channel Kir3.2
, Potassium channel, inwardly rectifying subfamily J member 6
, potassium channel-like protein