Potassium two pore domain channel subfamily K member 2 (KCNK2)

Potassium two pore domain channel subfamily K member 2 (KCNK2), commonly known as **TREK-1**, is a lipid- and mechanically-gated two-pore-domain potassium (*K2P*) channel that contributes to the regulation of resting membrane potential and membrane excitability in neurons and other cells[1][2][4]. It is predominantly expressed in the brain, heart, and other tissues, and plays critical roles in neuroprotection, anesthesia, pain modulation, and potentially psychiatric conditions. This channel responds to stimuli such as mechanical stretch, internal acidity, heat, and lipid environment, and can be activated by certain anesthetics and neuroactive drugs[1][2][4]. KCNK2/TREK-1 is considered a valid therapeutic target for neurological, neuropsychiatric, and inflammatory diseases, with pharmacological modulation impacting neuronal activity, pain signaling, and blood-brain barrier function[1][3][4].

Other names

TREK-1K2P2.1TREKTREK1TPKC1Two pore domain potassium channel TREK-1Outward rectifying potassium channel protein TREK-1Potassium inwardly-rectifying channel subfamily K member 2Tandem-pore-domain potassium channel TREK-1TWIK-related potassium channel 1Two-pore potassium channel 1hTREK-1chTREK-1ePotassium channel subfamily K member 2

Channel activation leads to hyperpolarization and reduced neuronal excitability (anesthetic, neuroprotective, antidepressant effects). Channel inhibition increases excitability (antidepressant action of fluoxetine). Mechanosensitive and lipid-gated modulation.