Cardiac KCNK (K2P) Channel Antibody Explorer Kit

K₂P channels are involved in various physiological and pathological processes including vascular and pulmonary hypertension, depression and cardiac arrhythmias. 

K₂P channels have two pore domains (P1 and P2) and form dimers thus creating a unit with four pore domains. Each pore domain is bordered by two membrane spanning helices (M1, M2, M3 and M4). The channel’s N- and C- termini are cytoplasmic and there is an extended extracellular loop between P1 and M1. This loop interacts with the same structure of the other subunit of the dimer and it contains a cysteine residue involved in the formation of a covalent bridge between the two subunits¹. TWIK1 channels are a subtype of K₂P channels that are expressed in the heart and primarily in atrial and purkinje fibers. TWIK1 mediate “background” potassium currents that participate in maintaining resting membrane potential.

At very low plasma K⁺ levels hypokalemia can cause severe cardiac arrhythmias leading to sudden death. One of the mechanisms for arrhythmia is a paradoxical depolarization of cardiac myocytes that can initiate the onset of arrhythmia. Recently, it was suggested that TWIK1 channels are involved in this pathological activity by changing ion selectivity and becoming more permeable to Na⁺ and conducting an inward current of Na⁺ under hypokalemic conditions. This inward leak is prolonged even after reaching K⁺ equilibrium and has a substantial effect on membrane resting potential².