Rabbit anti-Human KCNJ3 Polyclonal Antibody

Uniprot Id

P48549

Target Species

Human

Target Name

KCNJ3

Target Full Name

G protein-activated inward rectifier potassium channel 1

Target Function

This potassium channel 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. This receptor plays a crucial role in regulating the heartbeat.

Target Subcellular Location

Membrane; Multi-pass membrane protein.

Target Protein Families

Inward rectifier-type potassium channel (TC 1.A.2.1) family, KCNJ3 subfamily

Target Research Area

Cardiovascular

Target Synonyms

KCNJ3; GIRK1; G protein-activated inward rectifier potassium channel 1; GIRK-1; Inward rectifier K(+ channel Kir3.1; Potassium channel, inwardly rectifying subfamily J member 3

Target Background

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 plays an important role in regulating heartbeat. It associates with three other G-protein-activated potassium channels to form a heteromultimeric pore-forming complex that also couples to neurotransmitter receptors in the brain and whereby channel activation can inhibit action potential firing by hyperpolarizing the plasma membrane. These multimeric G-protein-gated inwardly-rectifying potassium (GIRK) channels may play a role in the pathophysiology of epilepsy, addiction, Down's syndrome, ataxia, and Parkinson's disease. Alternative splicing results in multiple transcript variants encoding distinct proteins.