Aliases for KCNJ10 Gene
- Potassium Inwardly Rectifying Channel Subfamily J Member 10 2 3 5
- Potassium Channel, Inwardly Rectifying Subfamily J Member 10 3 4
- ATP-Dependent Inwardly Rectifying Potassium Channel Kir4.1 3 4
- ATP-Sensitive Inward Rectifier Potassium Channel 10 3 4
- Inward Rectifier K(+) Channel Kir1.2 3 4
- Glial ATP-Dependent Inwardly Rectifying Potassium Channel KIR4.1 3
- Potassium Inwardly-Rectifying Channel, Subfamily J, Member 10 2
- Potassium Voltage-Gated Channel Subfamily J Member 10 3
External Ids for KCNJ10 Gene
Previous GeneCards Identifiers for KCNJ10 Gene
This gene encodes a member of the inward rectifier-type potassium channel family, characterized by having a greater tendency to allow potassium to flow into, rather than out of, a cell. The encoded protein may form a heterodimer with another potassium channel protein and may be responsible for the potassium buffering action of glial cells in the brain. Mutations in this gene have been associated with seizure susceptibility of common idiopathic generalized epilepsy syndromes. [provided by RefSeq, Jul 2008]
GeneCards Summary for KCNJ10 Gene
KCNJ10 (Potassium Inwardly Rectifying Channel Subfamily J Member 10) is a Protein Coding gene. Diseases associated with KCNJ10 include Seizures, Sensorineural Deafness, Ataxia, Mental Retardation, And Electrolyte Imbalance and Deafness, Autosomal Recessive 4, With Enlarged Vestibular Aqueduct. Among its related pathways are Inwardly rectifying K+ channels and Transmission across Chemical Synapses. Gene Ontology (GO) annotations related to this gene include identical protein binding and potassium channel activity. An important paralog of this gene is KCNJ15.
UniProtKB/Swiss-Prot Summary for KCNJ10 Gene
May be responsible for potassium buffering action of glial cells in the brain. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium (By similarity). In the kidney, together with KCNJ16, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules.
The inward-rectifier potassium channel family (also known as 2-TM channels) include the strong inward-rectifier channels (Kir2.x), the G-protein-activated inward-rectifier channels (Kir3.x) and the ATP-sensitive channels (Kir6.x), which combine with sulphonylurea receptors.