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

Function

May be responsible for potassium buffering action of glial cells in the brain (PubMed:7608203). 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 (PubMed:7608203). 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

Predominantly expressed in the brain, including in glial cells of the cerebellum and forebrain. Expressed at lower levels in the kidney, and other peripheral tissues

Subunit

Homotetramer (PubMed:38355723). 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 (By similarity)

• Takumi T. et al. A novel ATP-dependent inward rectifier potassium channel expressed predominantly in glial cells. — J. Biol. Chem. (1995)
• Bond C.T. et al. Cloning and expression of a family of inward rectifier potassium channels. — Recept. Channels (1994)
• Bredt D.S. et al. Cloning and expression of two brain-specific inwardly rectifying potassium channels. — Proc. Natl. Acad. Sci. U.S.A. (1995)
• Rapedius M. et al. Control of pH and PIP2 gating in heteromeric Kir4.1/Kir5.1 channels by H-Bonding at the helix-bundle crossing. — Channels (2007)
• Sala-Rabanal M. et al. Molecular mechanisms of EAST/SeSAME syndrome mutations in Kir4.1 (KCNJ10). — J. Biol. Chem. (2010)
• Zhou X. et al. Pharmacological inhibition of Kir4.1 evokes rapid-onset antidepressant responses. — Nat. Chem. Biol. (2024)