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|Tested species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A synthetic peptide derived from the C-terminal region of human KCNJ5|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.4, with 50% glycerol, 150mM NaCl|
|Contains||0.02% sodium azide|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:500-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
G protein-coupled inwardly rectifying potassium channels (Kir3.1 through Kir3.4) are coupled to numerous neurotransmitter receptors in the brain and are abundantly expressed in the olfactory bulb, hippocampus, neocortex, dentate gyrus, cerebellar cortex and thalamus regions of the brain. Also known as GIRK, Kir3 potassium channels localize to the soma and dendrites as well as axons of neurons. Liberated Gbg subunits from G protein heterotrimers bind to and regulate Kir3 channel activity. Gb3- and Gb4-containing Gbg dimers bind directly to cytoplasmic domains of Kir3 proteins and increase the K+ current while Gb5-containing Gbg dimers inhibit Kir3 K+ current. Kir3 activity is also inhibited by tyrosine phosphorylation. Brain-derived neurotrophic factor activates receptor tyrosine kinase B, which then phosphorylates Kir3 tyrosine residues, effectively inactivating the Kir3 channels.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
cardiac ATP-sensitive potassium channel; CIR; GIRK4; heart KATP channel; inward rectifier K+ channel KIR3.4; inwardly rectifying subfamily J member 5; IRK-4; IRK4; KATP1; KCNJ5; Potassium channel; potassium channel, inwardly rectifying subfamily J, member 5; potassium inwardly-rectifying channel, subfamily J, member 5
CIR; GIRK4; KATP1; KCNJ5; KIR3.4; LQT13