Overview
- Peptide (C)YEQLMNEYNKANSPKGT, amino acid residues 483-499 of human KCNK5 (Accession number O95279). Intracellular, C-terminus.
- Rat kidney membranes (1:200).
Mouse Ehrlich ascites tumour (EAT) cells (1:250) (Kirkegaard, S.S. et al. (2013) Cell. Physiol. Biochem. 32, 1238.). 
Western blot analysis of rat kidney membranes:1. Anti-KCNK5 (TASK-2) Antibody (#APC-037), (1:200).
2. Anti-KCNK5 (TASK-2) Antibody, preincubated with KCNK5/TASK-2 Blocking Peptide (#BLP-PC037).
- Rat kidney and pancreas sections.
KCNK5 (also named TWIK-related acid sensitive K+ channel 2, TASK-2 or K2P5.1) is a member of the 2-pore (2P) domain K+ channels family that includes at least 16 members. These channels show little time- or voltage-dependence and are considered to be “leak” or “background” K+ channels, thereby generating background currents which help set the membrane resting potential and cell excitation.
The K2P channels have a signature topology that includes four transmembrane domains and two pore domains with intracellular N- and C- termini. The functional channel is believed to be a dimer.
K2P channels are regulated by diverse physical and chemical stimuli including temperature, changes in intracellular pH, mechanical stretch, inhalation anesthetics, etc. The channels can then be subclassified based in their specific activators.
As indicated by its name, KCNK5 (K2P5.1) is sensitive to variations in external pH. KCNK5 current is maximal at pH 8.8 but it is only 10% at pH 6.5.
The channel is expressed in several epithelial tissues including pancreas, lung, small intestine and specially kidney. In the kidney KCNK5 has an important function in NaHCO3 absorption in the proximal tubule as knockout mice for KCNK5 display metabolic acidosis and hypotension.
