Ion channel that contributes to passive transmembrane potassium transport. Reversibly converts between a voltage-insensitive potassium leak channel and a voltage-dependent outward rectifying potassium channel in a phosphorylation-dependent manner. In astrocytes, forms mostly heterodimeric potassium channels with KCNK1, with only a minor proportion of functional channels containing homodimeric KCNK2 (PubMed:24496152). In astrocytes, the heterodimer formed by KCNK1 and KCNK2 is required for rapid glutamate release in response to activation of G-protein coupled receptors, such as F2R and CNR1 (PubMed:24496152). Inhibited by barium (PubMed:9003761). Activated by volatile general anesthetics such as chloroform, diethyl ether, halothane and isoflurane (PubMed:10321245). Channel activation is extremely rapid (PubMed:9003761). Single channel conductance is about 14 pS (PubMed:9003761). Homodimer; disulfide-linked (PubMed:24496152). Heterodimer with KCNK1; disulfide-linked (PubMed:24496152). Interacts with BVES; the interaction enhances KCNK2 surface expression and is inhibited by cAMP (PubMed:22354168, PubMed:26642364). Location at the cell membrane requires interaction with KCNK1. Is not detected at the cell membrane when KCNK1 is absent. Detected in hippocampus astrocytes (at protein level) (PubMed:24496152). High expression in brain and lung. Also detected in kidney, heart and skeletal muscle. Not detected in liver. In the brain, highest expression in olfactory bulb, hippocampus and cerebellum. Phosphorylation at Ser-348 controls the reversible conversion from a leak channel to a voltage-dependent channel. Belongs to the two pore domain potassium channel (TC 1.A.1.8) family.