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This receptor is controlled by G proteins. Zusätzlich bieten wir Ihnen Potassium Inwardly-Rectifying Channel, Subfamily J, Member 9 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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This study is the first to identify the expression of GIRK2 (zeige KCNJ6 Antikörper)-4 subunits in human esophageal smooth muscle cells.
a decisive role for the neuronal K(+) channel (zeige KCNC4 Antikörper) in regulating NCAM (zeige NCAM1 Antikörper)-dependent neurite outgrowth and attribute a physiologically meaningful role to the functional interplay of Kir3.3, NCAM (zeige NCAM1 Antikörper), and TrkB (zeige NTRK2 Antikörper) in ontogeny
The frequencies of GRIK3 (zeige GRIK3 Antikörper) (T928G) genotype distributions in the patients with schizophrenia were similar to those of their relatives.
GIRK1 (zeige KCNJ3 Antikörper) and GIRK2 (zeige KCNJ6 Antikörper) channels, but not GIRK3 or GIRK4 (zeige KCNJ5 Antikörper), may may activate signaling pathways in development of lung cancer
GIRK-3 knock-out mice show significant ethanol conditioned place preference and reward compared to wild-type littermates.
GIRK3 appears to be a critical gatekeeper of ethanol incentive salience and a potential target for the treatment of excessive ethanol consumption.
GIRK3 exhibited in Purkinje neurons, basket cells, stellate cells and unipolar brush cells.
A single locus is partially responsible for the genetic mediation of pain inhibition, and genetic variation associated with the potassium channel (zeige KCNAB2 Antikörper) gene, Kcnj9, is a prime candidate for explaining the variable response to these analgesic drugs.
Inhibition of adrenergic tone is required for the induction of dependence, and channels containing GIRK2 (zeige KCNJ6 Antikörper) and GIRK3 serve as inhibitory gate.
Results describe opioid-induced postsynaptic inhibition in locus coeruleus neurons from wild-type and GIRK2 (zeige KCNJ6 Antikörper)/GIRK3(-/-) mice at baseline and following chronic morphine treatment.
Kcnj9 as a particularly promising candidate and report the development of a Kcnj9-null mutant model that exhibits significantly less severe withdrawal from pentobarbital as well as other sedative-hypnotics.
This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium\; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium (By similarity).
potassium inwardly-rectifying channel subfamily J9
, G protein-activated inward rectifier potassium channel 3
, potassium inwardly-rectifying channel, subfamily J, member 9
, G protein-coupled inward rectifier potassium channel
, inward rectifier K(+) channel Kir3.3
, inwardly rectifier K+ channel KIR3.3
, potassium channel, inwardly rectifying subfamily J member 9
, inwardly rectifier K(+) channel Kir3.3