Voltage-gated potassium channel that plays an important role in the rapid repolarization of fast-firing brain neurons. The channel opens in response to the voltage difference across the membrane, forming a potassium-selective channel through which potassium ions pass in accordance with their electrochemical gradient. The channel displays rapid activation and inactivation kinetics (PubMed:18539595, PubMed:26997484, PubMed:24218544). It plays a role in the regulation of the frequency, shape and duration of action potentials in Purkinje cells (PubMed:15217387, PubMed:18448641, PubMed:24218544). Required for normal survival of cerebellar neurons, probably via its role in regulating the duration and frequency of action potentials that in turn regulate the activity of voltage-gated Ca(2+) channels and cellular Ca(2+) homeostasis (PubMed:24218544). Required for normal motor function (PubMed:16923152, PubMed:18448641). Plays a role in the reorganization of the cortical actin cytoskeleton and the formation of actin veil structures in neuronal growth cones via its interaction with HAX1 and the Arp2/3 complex (PubMed:26997484). Homotetramer. Heterotetramer with KCNC1 (By similarity). Interacts (via C-terminus) with HAX1. Identified in a complex with ACTR3, a subunit of the Arp2/3 complex; this interaction is indirect and depends on the presence of HAX1. Interaction with HAX1 modulates channel gating (PubMed:26997484). Detected on Purkinje cell dendritic spines, positioned perisynaptically but also in extrasynaptic positions along the spine membranes (By similarity). Detected at presynaptic calices of Held (PubMed:26997484). Colocalizes with the cortical actin cytoskeleton and the Arp2/3 complex (By similarity). Detected on Purkinje cells in the dentate, interposed and medial nucleus in cerebellum (PubMed:15217387, PubMed:18448641). Detected in brainstem (PubMed:18539595). Detected at calyces of Held in the auditory brain stem (at protein level) (PubMed:26997484). Isoform KV3.3B is highly enriched in the brain, particularly in the cerebellum, where its expression is confined to Purkinje cells and deep cerebellar nuclei. Isoform KV3.3A is not expressed in cerebellum. Expression begins in cerebellar Purkinje cells between postnatal day 8 (P8) and P10 and continues through adulthood. The segment S4 is probably the voltage-sensor and is characterized by a series of positively charged amino acids at every third position. The cytoplasmic N-terminus mediates N-type inactivation. The C-terminal cytoplasmic tail contributes to the regulation of channel inactivation and to the interaction with HAX1 and the Arp2/3 complex. N-glycosylated. Mice lacking both Kcnc3 and Kcnc1 are born at the expected Mendelian rate, but the pups do not thrive and all die about 26 days after birth when kept together with other littermates. Their failure to thrive may be due to motor problems; mutant pups survive when fed separately, but 45 days after birth their body weight is only 50 to 60 % of that of wild-type (PubMed:11517255). They appear uncoordinated and display severe ataxia, myoclonus and spontaneous whole-body muscle jerks, but display no obvious alterations in brain morphology (PubMed:11517255, PubMed:15217387, PubMed:16923152). Mice lacking only Kcnc3 still display ataxic gait and decreased motor skill, but to a lesser degree than mice lacking both Kcnc3 and Kcnc1 (PubMed:16923152, PubMed:18448641). Purkinje cell-specific expression of Kcnc3 restores normal motor skills (PubMed:18448641). Mutant mice are also much more sensitive to ethanol and fall sideways at ethanol concentrations that have no effect on wild-type mice (PubMed:11517255). They display increased locomotor and exploratory activity (PubMed:11517255, PubMed:15217387). Mice lacking Kcnc3 or both Kcnc3 and Kcnc1 are resistant to the tremorogenic agent harmaline (PubMed:15217387). Belongs to the potassium channel family. C (Shaw) (TC 1.A.1.2) subfamily. Kv3.3/KCNC3 sub-subfamily. Probable cloning artifact. Incorrect C-terminus.