SCUBA

KCNC3 — Potassium voltage-gated channel subfamily C member 3

KCNC3 belongs to a gene co-expression module in 1 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

KCNC3's module in each cell type

Cell typeModuleShares the module with
Hematopoietic progenitor cellsMyeloid Innate Immune
Myeloid development
CCR2, CUX2, CYBB, FXYD7, KIF17, NFKB1, PLD4, RNASE6 +5 more

About the gene

SynonymsKv3.3, SCA13
Chromosome19: 50311937-50333515
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classDisease related genes, FDA approved drug targets, Human disease related genes, Predicted intracellular proteins, Predicted membrane proteins, Transporters, Voltage-gated ion channels
Molecular functionIon channel, Potassium channel, Voltage-gated channel
Biological processIon transport, Potassium transport, Transport

Function

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. It plays a role in the regulation of the frequency, shape and duration of action potentials in Purkinje cells. 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 (By similarity). Required for normal motor function. 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.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.