|Application ||WB, IP|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||126655 Da|
|Homology||Rabbit - identical; dog - 51/54 amino acid residues identical;mouse, rat - 50/54 amino acid residues identical.|
|Other Names||Potassium voltage-gated channel subfamily H member 2, Eag homolog, Ether-a-go-go-related gene potassium channel 1, ERG-1, Eag-related protein 1, Ether-a-go-go-related protein 1, H-ERG, hERG-1, hERG1, Voltage-gated potassium channel subunit Kv111, KCNH2, ERG, ERG1, HERG|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||GST fusion protein with sequence DSLSQVSQFMACEELPPGAPELPQEGPTRRLSLPGQLGALTSQPLHRHGSDPGS, corresponding to amino acid residues 1106-1159 of humanֲ Kv11.1 (HERG) (Accession Q12809), (MW: 35 kDa.). Intracellular, C-terminus.The antibody recognizes the HERG1b splice variant but not splice variants HERG1-3 and HERG-4|
|Peptide Confirmation||Confirmed by DNA sequence and SDS-PAGE.|
|Application Details||Western blot analysis (WB): - HEK 293 cells transfected with hERG (see Varkevisser, R. et al. (2013) in Product Citations). - Neonatal rat ventricular myocytes (NRVMs) (see Dennis, A.T. et al. (2011) in Product Citations). Immunoprecipitation (IP): - HeLa cells transfected with hERG (see Apaja, P.M. et al. (2013) in Product Citations). Immunohistochemistry (IH): - Mouse frozen heart sections (1:300) (see Teng, G.Q. et al. (2008) in Product Citations). Immunocytochemistry (IC): - HEK 293 cells transfected with hERG (see Varkevisser, R. et al. (2013) in Product Citations).|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.6 mg/ml.|
|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 PBS.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||3 µg fusion protein per 1 µg antibody.|
|Formulation||Lyophilized powder. Phosphate buffered saline (PBS), pH 7.4, 1 % BSA, 0.025% NaN3.|
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Provided below are standard protocols that you may find useful for product applications.
The KV11.1 (HERG) channel is a member of the ether-a-go-go (EAG) subfamily of voltage-dependent K+ channels that includes the related proteins KV11.2 and KV11.3 (erg2 and erg3). KV11.1 possess the signature structure of the voltage-dependent K+ channels: six membrane-spanning domains and intracellular N and C termini. The KV11.1 current is characterized by strong inward rectification with slow activation and very rapid inactivation kinetics. The channel is expressed in the brain and heart (where it underlies the IKr current) and has a central role in mediating repolarization of action potentials.1,2 Mutations in the KV11.1 channel cause inherited long QT syndrome (LQTS) or abnormalities in the repolarization of the heart that are associated with life-threatening arrhythmias and sudden death. All the identified KV11.1 mutations produce loss of function of the channel via several cellular mechanisms ranging from alterations of gating properties, alterations of channel permeability/selectivity and alterations in intracellular channel trafficking that decreases the number of channels that reach the cell membrane.1,2 Lately drug-induced forms of LQTS have been reported for a wide range of non-cardiac drugs including antihistamines, psychoactive agents and antimicrobials. All these drugs potently block the KV11.1 channel as an unintended side effect, prompting regulatory drug agencies to issue recommendations for the testing of new drugs for their potential KV11.1 blocking effect. In addition, KV11.1 expression was found to be upregulated in several tumor cell lines of different histogenesis suggesting that it confers the cells some advantage in cell proliferation. Indeed, in several studies it has been shown that inhibition of the KV11.1 current leads to a decrease in tumor cell proliferation.3 Several toxins from scorpion venoms are potent blockers (affecting the channels in the nanomolar range) of KV11.1channels. Among these the most potent and selective are Ergtoxin-1 (#RTE-450), (16 nM)4 and BeKM-1 (#RTB-470), (3 nM).5 In addition, the methanesulfonanilide class III antiarrhythmic agent E-4031 (#E-500), also blocks KV11.1 channel in the nanomolar range (7.7 nM).6
References 1. Curran, M.E. et al. (1995) Cell 80, 795 2. Sanguinetti, M.C. et al. (1995) Cell 81, 299. 3. Pardo, L.A. et al. (2004) Physiology 19, 285. 4. Gurrola, G.B. et al. (1999) FASEB. J. 13, 953. 5. Korolkova, Y.V. et al. (2001) J. Biol. Chem. 276, 9868. 6. Zhou, Z. et al. (1998) Biophys.J. 74, 230.
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