Thermo Fisher Scientific Kir3.4 (KCNJ5) Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:500-1:1,000

-

Immunocytochemistry (ICC/IF)

1:100-1:500

-

Product Specifications

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

A synthetic peptide derived from the C-terminal region of human KCNJ5 if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:Kir3.4 (KCNJ5),uniProtId:P48544-1,ncbiNodeId:9606,antigenRange:419,antigenLength:419,antigenImageFileName:PA5-39617_Kir3.4_KCNJ5_P48544-1_Rabbit.svg,antigenImageFileNamePDP:PA5-39617_Kir3.4_KCNJ5_P48544-1_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

View immunogen .st0{fill:#FFFFFF;} .st1{fill:#1E8AE7;}

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Storage conditions

-20°C

Shipping conditions

Wet ice

RRID

AB_2556169

Target Information

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.