|Calculated MW||47093 Da|
|Homology||Rat - identical; mouse - 17/18 amino acidresidues identical.|
|Other Names||Potassium channel subfamily K member 2, 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, TREK, TREK1|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide DPKSAAQNSKPRLSFSTK(C), corresponding to residues 8-25 of human K2P2.1 (TREK-1) (Accession O95069).ֲ ֲ Intracellular, N-terminus.|
|Peptide Confirmation||Confirmed by mass-spectrography and amino acid analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.025% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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K2P2.1 (also named TWIK-Related K+ channel, TREK-1 or KCNK2) 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. 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. K2P2.1 can be integrated to a K2P subfamily that includes K2P4.1 (TRAAK) and K2P10.1 (TREK2) that are activated by intracellular unsaturated fatty acids such as arachidonic acid, lysophosphatidic acid and mechanical stretch. In addition, K2P2.1 can also be activated by general anesthetics such as halothane and chloroform and intracellular acidification. K2P2.1 expression in humans is largely restricted to the brain with some expression in ovary and small intestine while K2P2.1expression in rodents is more widespread. K2P2.1 has an important role in mood regulation, as knockout mice show resistance to depression, suggesting that K2P2.1 may be a potential target for anti-depressants. K2P2.1 is involved in the fast release of glutamate from astrocytes. It requires the activation of Gαi, dissociation of Gβγ, followed by the opening of the glutamate permeable K2P2.1 (TREK-1) K+ channel through its interaction with Gβγ. For this purpose, TREK-1 is localized at the cell surface of the cell body and processes of astrocytes. Abgent is pleased to offer a highly specific antibody directed against an epitope of human K2P2.1. Anti-K2P2.1 (TREK-1) antibody (#AG1125) can be used in western blot analysis, and has been designed to recognize TREK-1 channel from mouse, rat and human samples.
References 1. Maingret, F. et al. (1999) J. Biol. Chem. 274, 26691. 2. Lesage, F. and Lazdunski, M. (2000) Am. J. Physiol. Renal Physiol. 279, F793. 3. Kim, D. (2003) Trends Pharmacol. Sci. 24, 648. 4. Heurteaux, C. et al. (2006) Nat. Neurosci. 9, 1134. 5. Woo, D.H. et al. (2012) Cell 151, 25.
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