Aliases for KCNJ9 Gene
- Potassium Voltage-Gated Channel Subfamily J Member 9 2 3
- Potassium Inwardly-Rectifying Channel, Subfamily J, Member 9 2 3
- Potassium Channel, Inwardly Rectifying Subfamily J, Member 9 3 5
- Potassium Channel, Inwardly Rectifying Subfamily J Member 9 3 4
- Inward Rectifier K(+) Channel Kir3.3 3 4
- GIRK-3 3 4
External Ids for KCNJ9 Gene
Previous GeneCards Identifiers for KCNJ9 Gene
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins. It associates with another G-protein-activated potassium channel to form a heteromultimeric pore-forming complex. [provided by RefSeq, Jul 2008]
GeneCards Summary for KCNJ9 Gene
KCNJ9 (Potassium Voltage-Gated Channel Subfamily J Member 9) is a Protein Coding gene. Diseases associated with KCNJ9 include Corneal Dystrophy, Schnyder Type. Among its related pathways are Inwardly rectifying K+ channels and G-Beta Gamma Signaling. GO annotations related to this gene include PDZ domain binding and G-protein activated inward rectifier potassium channel activity. An important paralog of this gene is KCNJ3.
UniProtKB/Swiss-Prot for KCNJ9 Gene
This receptor is controlled by G proteins. 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 (By similarity).
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.