Recombinant Mouse ATP-sensitive inward rectifier potassium channel 10 (Kcnj10) Protein

Function

May be responsible for potassium buffering action of glial cells in the brain (By similarity). 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 (By similarity)

Subcellular Location

Membrane (Multi-pass membrane protein); Basolateral cell membrane

Tissue Specificity

Widely expressed in adult brain, including in the neocortex, the stratum pyrimadale of the hippocampus and the piriform cortex. Expressed by cultured astrocytes and also by cocultured cortical neurons (at protein level). In the distal segment of the nephron, expressed in the distal convoluted tubule, the connecting tubule, and the early cortical collecting duct (PubMed:19420365, PubMed:33811157)

Subunit

Homotetramer (By similarity). In kidney cells, it forms heteromeric channels with Kir5.1/KCNJ16; this interaction is required for KCNJ16 localization to the basolateral membrane. Interacts with MAGI1, alone and possibly as a heteromer with KCNJ16; this interaction may facilitate KCNJ10/KCNJ16 potassium channel expression at the basolateral membrane in kidney cells (By similarity). Interacts with PATJ (PubMed:9647694)

• Inanobe A. et al. PubMed: CI-4CDIFR1KRRF0I (MAR-)
• Li L. et al. Identification of an inward rectifier potassium channel gene expressed in mouse cortical astrocytes. — Glia (2001)
• Kurschner C. et al. CIPP, a novel multivalent PDZ domain protein, selectively interacts with Kir4.0 family members, NMDA receptor subunits, neurexins, and neuroligins. — Mol. Cell. Neurosci. (1998)
• Bockenhauer D. et al. Epilepsy, ataxia, sensorineural deafness, tubulopathy, and KCNJ10 mutations. — N. Engl. J. Med. (2009)
• Huttlin E.L. et al. A tissue-specific atlas of mouse protein phosphorylation and expression. — Cell (2010)
• Schlingmann K.P. et al. Defects in KCNJ16 cause a novel tubulopathy with hypokalemia, salt wasting, disturbed acid-base homeostasis, and sensorineural deafness. — J. Am. Soc. Nephrol. (2021)