Inward rectifying K⁺ (K_ir) channels generate under physiological conditions, large K⁺ conductance at potentials negative to Ek but permit less current flow at potentials positive to Ek.

K_ir3.2 (also known as GIRK2 or KCNJ6) belongs to a G-protein gated subfamily of K_ir channels. K_ir3.2 is one of four subunits (K_ir3.1, K_ir3.3 and K_ir3.4) that form functional tetrameric K_G channel assemblies. K_G channels are activated by GTP (GTPi) in the presence of an agonist or by intracellular GTPγS in the absence of an agonist. There are at least four different isoforms of K_ir3.2 which are generated by alternative splicing from a single gene. K_ir3.2 isoforms exhibit differential expression patterns in various tissues such as brain, pituitary, pancreas, and testis, where they usually coincide with the expression of other K_ir3.x subunits.

K_ir3.2 is expressed on the cell surface due to two forward trafficking signal in its cytoplasmic region. One is an ER export signal in its NH2 terminus and the other is a post-ER trafficking signal that is composed of a cluster of acidic residues in the COOH terminus.

Knockout of K_ir3.2 is accompanied by a decrease in K_ir3.1 protein expression in the brain, the development of spontaneous seizures, and a range of phenotypes related to sporadic seizures¹.