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This receptor is controlled by G proteins. Additionally we are shipping Potassium Inwardly-Rectifying Channel, Subfamily J, Member 9 Proteins (6) and many more products for this protein.
Showing 10 out of 44 products:
Human Polyclonal KCNJ9 Primary Antibody for WB - ABIN2776176
Ji, Foo, ORoak, Zhao, Larson, Simon, Newton-Cheh, State, Levy, Lifton: Rare independent mutations in renal salt handling genes contribute to blood pressure variation. in Nature genetics 2008
Rat (Rattus) Polyclonal KCNJ9 Primary Antibody for WB - ABIN1742030
Williams: Modulation and block of ion channels: a new biology of polyamines. in Cellular signalling 1997
Human Polyclonal KCNJ9 Primary Antibody for ELISA, WB - ABIN1534917
Gregory, Barlow, McLay, Kaul, Swarbreck, Dunham, Scott, Howe, Woodfine, Spencer, Jones, Gillson, Searle, Zhou, Kokocinski, McDonald, Evans, Phillips, Atkinson, Cooper, Jones, Hall, Andrews, Lloyd et al.: The DNA sequence and biological annotation of human chromosome 1. ... in Nature 2006
This study is the first to identify the expression of GIRK2 (show KCNJ6 Antibodies)-4 subunits in human esophageal smooth muscle cells.
a decisive role for the neuronal K(+) channel (show KCNC4 Antibodies) in regulating NCAM (show NCAM1 Antibodies)-dependent neurite outgrowth and attribute a physiologically meaningful role to the functional interplay of Kir3.3, NCAM (show NCAM1 Antibodies), and TrkB (show NTRK2 Antibodies) in ontogeny
The frequencies of GRIK3 (show GRIK3 Antibodies) (T928G) genotype distributions in the patients with schizophrenia were similar to those of their relatives.
GIRK1 (show KCNJ3 Antibodies) and GIRK2 (show KCNJ6 Antibodies) channels, but not GIRK3 or GIRK4 (show KCNJ5 Antibodies), 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 (show KCNAB2 Antibodies) 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 (show KCNJ6 Antibodies) and GIRK3 serve as inhibitory gate.
Results describe opioid-induced postsynaptic inhibition in locus coeruleus neurons from wild-type and GIRK2 (show KCNJ6 Antibodies)/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