Recombinant Human Inward rectifier potassium channel 16 (KCNJ16) Protein

Function

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. KCNJ16 may be involved in the regulation of fluid and pH balance. In the kidney, together with KCNJ10, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules (PubMed:24561201)

Subcellular Location

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

Disease Association

Hypokalemic tubulopathy and deafness (HKTD) : An autosomal recessive disease characterized by renal tubulopathy with hypokalemia, salt wasting, disturbed acid-base homeostasis, and sensorineural deafness. [The disease is caused by variants affecting the gene represented in this entry]

Tissue Specificity

Widely expressed, with highest levels in adult and fetal kidney (at protein level). In the kidney, expressed in the proximal and distal convoluted tubules, but not in glomeruli nor collecting ducts

Subunit

It forms heteromeric channels with Kir4.1/KCNJ10; this interaction is required for KCNJ16 localization to the basolateral membrane in kidney cells. As a heteromer with KCNJ10, may interact with MAGI1; this interaction may facilitate KCNJ10/KCNJ16 potassium channel expression at the basolateral membrane in kidney cells (PubMed:24561201). May form heteromers with Kir2.1/KCNJ2 (Probable). Can form heteromeric channels with Kir4.2/KCNJ15 (By similarity)

• Liu Y. et al. The human inward rectifier K(+) channel subunit kir5.1 (KCNJ16) maps to chromosome 17q25 and is expressed in kidney and pancreas. — Cytogenet. Cell Genet. (2000)
• Derst C. et al. Genetic and functional linkage of Kir5.1 and Kir2.1 channel subunits. — FEBS Lett. (2001)
• Tanemoto M. et al. Mislocalization of K+ channels causes the renal salt wasting in EAST/SeSAME syndrome. — FEBS Lett. (2014)
• 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)