KCNJ10
KCNJ10 (potassium inwardly rectifying channel subfamily J member 10, also known as Kir4.1 and Kir1.2) is an ATP-sensitive inward rectifier potassium channel. It may buffer potassium in glial cells of the brain and mediates basolateral potassium recycling in the kidney. Browse Assay Genie's current range of KCNJ10 research reagents below, or read on for the biology behind the target.
KCNJ10 belongs to the inward rectifier-type potassium channel family, whose members allow potassium to flow into the cell more readily than out of it. The voltage dependence of the channel is regulated by extracellular potassium: as external potassium rises, the voltage range of channel opening 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 extracellular barium and cesium.
In the brain, KCNJ10 may be responsible for the potassium buffering action of glial cells. In the kidney, together with KCNJ16, it mediates basolateral K(+) recycling in distal tubules, a process that is critical for Na(+) reabsorption at the tubules. The protein localises to the basolateral cell membrane. The NCBI Gene summary notes that the encoded protein may form a heterodimer with another potassium channel protein.
The KCNJ10 gene is assigned by HGNC to the potassium inwardly rectifying channel subfamily J group, and the protein is also known as Kir4.1 and Kir1.2. Its previous HGNC name was potassium inwardly-rectifying channel, subfamily J, member 10. Mutations in the gene have been associated with seizure susceptibility in common idiopathic generalised epilepsy syndromes. Orthologous genes are named Kcnj10 in mouse and rat.
KCNJ10 may be responsible for the potassium buffering action of glial cells in the brain, making it a focus for studies of glial function.
With KCNJ16, KCNJ10 mediates basolateral K(+) recycling in distal tubules, which is critical for Na(+) reabsorption.
Mutations in the KCNJ10 gene have been associated with seizure susceptibility in common idiopathic generalised epilepsy syndromes.
Its inward rectification, magnesium block and sensitivity to extracellular potassium, barium and cesium make it a model for rectifier channel behaviour.
KCNJ10 forms an inward rectifier potassium channel that lets potassium enter cells more readily than leave them. It may provide potassium buffering in brain glial cells and, with KCNJ16, mediates basolateral K(+) recycling in kidney distal tubules, which supports Na(+) reabsorption.
KCNJ10 is also called Kir4.1 and Kir1.2. Its full HGNC name is potassium inwardly rectifying channel subfamily J member 10, and UniProt lists it as ATP-sensitive inward rectifier potassium channel 10. Searching under any of these names should find the same target.
Mutations in the KCNJ10 gene have been associated with seizure susceptibility in common idiopathic generalised epilepsy syndromes. Orthologues exist in mouse and rat, both named Kcnj10; 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 P78508; product specifications from Assay Genie datasheets.