KCNJ5
KCNJ5 is a G protein-controlled inward rectifier potassium channel subunit, also known as Kir3.4 and GIRK4. It allows potassium to flow into the cell more readily than out of it, and the gene has also been referred to as CIR, KATP1 and LQT13. Browse Assay Genie's current range of KCNJ5 research reagents below, or read on for the biology behind the target.
KCNJ5 encodes a member of the inward rectifier-type potassium channel family. Inward rectifier channels are characterised by a greater tendency to let potassium flow into the cell than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium: as external potassium is raised, the voltage range over which the channel opens shifts to more positive voltages. Inward rectification is mainly due to blockage of outward current by internal magnesium, and the channel can be blocked by external barium. This channel is controlled by G proteins.
The KCNJ5 gene encodes an integral membrane protein that belongs to one of seven subfamilies of inward-rectifier potassium channel proteins, termed potassium channel subfamily J. The encoded protein is a subunit of a potassium channel that is homotetrameric. UniProt places it in the KCNJ5 subfamily of the inward rectifier-type potassium channel family, and lists the protein name as G protein-activated inward rectifier potassium channel 4. Researchers working with the KCNJ5 protein will often encounter it under the names Kir3.4 or GIRK4.
Naturally occurring mutations in the KCNJ5 gene are associated with aldosterone-producing adenomas. The symbol LQT13 appears among its aliases, and the gene was previously named potassium inwardly-rectifying channel, subfamily J, member 5. Mouse and rat both have a Kcnj5 ortholog, which supports comparative studies of channel function and G protein regulation.
KCNJ5 is a useful model for studying inward rectification, including regulation by extracellular potassium, block by internal magnesium and sensitivity to external barium.
As a channel controlled by G proteins, KCNJ5 links receptor-driven G protein signalling to potassium flux across the membrane.
Naturally occurring KCNJ5 mutations are associated with aldosterone-producing adenomas, making the gene relevant to studies of these tumours.
The protein forms a homotetrameric potassium channel, so KCNJ5 supports work on subunit composition within the potassium channel subfamily J.
KCNJ5 encodes a subunit of an inward rectifier potassium channel that allows potassium to flow into the cell more readily than out. The channel is controlled by G proteins, and its opening is shifted by extracellular potassium concentration. Internal magnesium blocks outward current.
KCNJ5 is also called Kir3.4 and GIRK4, with CIR, KATP1 and LQT13 listed as further aliases. UniProt names the protein G protein-activated inward rectifier potassium channel 4. HGNC gives the full name as potassium inwardly rectifying channel subfamily J member 5.
Naturally occurring mutations in the KCNJ5 gene are associated with aldosterone-producing adenomas. Mouse and rat each carry a Kcnj5 ortholog. Check the datasheet of any product for its validated reactivity.
Other members of the potassium inwardly rectifying channel subfamily J with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P48544; product specifications from Assay Genie datasheets.