KCNT2

Outward rectifying potassium channel. Produces rapidly activating outward rectifier K(+) currents. Activated by high intracellular sodium and chloride levels. Channel activity is inhibited by ATP and by inhalation anesthetics, such as isoflurane (By similarity). Inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1.

Full Name

potassium channel, subfamily T, member 2

Function

Outward rectifying potassium channel. Produces rapidly activating outward rectifier K(+) currents. Activated by high intracellular sodium and chloride levels (PubMed:14684870, PubMed:16687497, PubMed:29069600).
Channel activity is inhibited by ATP and by inhalation anesthetics, such as isoflurane (PubMed:16687497) (By similarity).
Inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRM1 (PubMed:16687497).

Biological Process

Potassium ion export across plasma membraneManual Assertion Based On ExperimentIMP:UniProtKB

Cellular Location

Cell membrane

Involvement in disease

Developmental and epileptic encephalopathy 57 (DEE57):
A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent. DEE57 is an autosomal dominant condition.

Topology

Cytoplasmic: 1-63
Helical: 64-84
Extracellular: 85-101
Helical: 102-122
Cytoplasmic: 123-137
Helical: 138-158
Extracellular: 159-164
Helical: 165-185
Cytoplasmic: 186-198
Helical: 199-219
Extracellular: 220-228
Pore-forming: 229-249
Extracellular: 250-256
Helical: 257-277
Cytoplasmic: 278-1135

PTM

Phosphorylated by protein kinase C. Phosphorylation of the C-terminal domain inhibits channel activity.