Introduction of KCNK2
KCNK2, the full name is potassium channel subfamily K member 2, also known as outward rectifying potassium channel protein TREK-1, TREK-1 K(+) channel subunit, two-pore domain potassium channel TREK-1, two-pore potassium channel TPKC1. KCNK2 is a member of the two-hole potassium (K2P) channel family. Human KCNK2 is highly expressed in the brain and is particularly abundant in interstitial neurons containing GABA (γ-aminobutyric acid) of the caudate nucleus and putamen. KCNK2 is also expressed in the prefrontal cortex, hippocampus, hypothalamus, midbrain serotonergic neurons of the dorsal raphe nucleus and sensory neurons of dorsal root ganglia (DRG). KCNK2 is also present in peripheral tissues such as gastrointestinal tracts. KCNK2 is a signal integrator that responds to a variety of physiological and pathological inputs.
|Basic Information of KCNK2|
|Protein Name||Potassium channel subfamily K member 2|
|Aliases||Outward rectifying potassium channel protein TREK-1, TREK-1 K(+) channel subunit, two-pore domain potassium channel TREK-1, two-pore potassium channel TPKC1|
|Organism||Homo sapiens (Human)|
Function of KCNK2 Membrane Protein
KCNK2 has complex gating and regulation by membrane receptors and second messengers and is central to ischemic and epileptic neuroprotection, pain perception and depression. In addition, KCNK2 is opened by neuroprotective agents, volatile and gaseous anesthetics, whereas it is inhibited by clinical doses of antidepressants, suggesting that the channel is an important pharmacological target. KCNK2 activity is stimulated by membrane stretching, heat, intracellular acidosis, and cellular lipids. Therefore, KCNK2 is qualified as a polymodal sensory ion channel that integrates a variety of physical and chemical stimuli. The C-terminal domain of this channel plays a major role in transducing of these stimuli into the channel opening. The proposed model suggests that the tight dynamic interaction of this domain with the inner leaflets of the plasma membrane is central to the mechanism of channel gating and regulation by membrane receptors and second messenger pathways.
Fig.1 Space-filling model of TREK-1 viewed from the cytosolic side. (Renigunta, 2015)
Application of KCNK2 Membrane Protein in Literature
Decreased atrial TREK-1 expression in atrial fibrillation patients with severe heart failure was verified in this article.
The decreased TREK-1 expression in the ganglia and ganglion intestine observed in Hirschsprung's disease (HSCR) may alter intestinal epithelial barrier function, leading to the development of enterocolitis.
TREK-1 overexpression inhibited CHO cell proliferation by inhibiting the activity of the PKA and p38/MAPK signaling pathways and subsequently inducing G1 phase cell arrest.
The expression of TREK1 was a benefit to restore intestinal epithelial barrier function in an allergic environment.
The data suggested that potassium channel protein TREK-1 (TREK-1) might be a biomarker in castration resistance free survival (CRFS) judgment of prostate cancer (PCa), as well as a potential therapeutic target.
KCNK2 Preparation Options
Membrane protein studies have advanced significantly over the past few years. Based on our versatile Magic™ membrane protein production platform, we could offer a series of membrane protein preparation services for worldwide customers in reconstitution forms or other protein forms in the same family. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-KCNK2 antibody development services.
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