KCNQ2, Monoclonal Antibody

Mouse Anti-Human KCNQ2 Monoclonal IgG1; KCNQ2 Antibody: Dylight 594; BFNC Antibody; EBN1 Antibody; ENB1 Antibody; HNSPC Antibody; KCNA11 Antibody; KQT like 2 Antibody; KV7.2 Antibody; KVEBN1. KvLQT2 Antibody; voltage gated potassium channel subunit Kv7.2 Antibody

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

IgG1

S26A-23

Mouse

Detects ~95 kDa.

Protein G Purified

PBS pH 7.4, 50% Glycerol, 0.09% Sodium Azide

1 mg/ml (lot specific)

Store at-20 degree C.

Small volumes of anti-KCNQ2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Kv7.2 (KvLQT2) is a potassium channel protein coded for by the gene KCNQ2. It is associated with benign familial neonatal convulsions (1).

Neuroscience; Ion Channels; Potassium Channels; Voltage-Gated Potassium Channels; Cancer

Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC), Immunofluorescence (IF), Immunoprecipitation (IP), Antibody Microarray (AM)

WB: 1:1000
IHC: 1:1000
ICC/IF: 1:100

Immunohistochemistry analysis using Mouse Anti-KCNQ2 Monoclonal Antibody, Clone S26A-23 at 1:1000 for 1 hour at RT. Secondary Antibody: HRP/DAB Detection System: Biotinylated Goat Anti-Mouse, Streptavidin Peroxidase, DAB Chromogen (brown) for 30 minutes at RT. Counterstain: Mayer Hematoxylin (purple/blue) nuclear stain at 250-500 ul for 5 minutes at RT.

Western Blot analysis of Human, hamster HEK and CHO cell lysates showing detection of KCNQ2 protein using Mouse Anti-KCNQ2 Monoclonal Antibody, Clone S26A-23 at 1:1000 for 2 hours at RT. Secondary Antibody: Sheep Anti-Mouse IgG: HRP for 1 hour at RT. KCNQ2 overexpressed.

Immunohistochemistry analysis using Mouse Anti-KCNQ2 Monoclonal Antibody, Clone S26A-23 at 1:1000 for 1 hour at RT. Secondary Antibody: FITC Goat Anti-Mouse (green) at 1:50 for 1 hour at RT.

potassium voltage-gated channel subfamily Q member 2

potassium voltage-gated channel subfamily KQT member 2

Potassium voltage-gated channel subfamily KQT member 2

KCNQ2_HUMAN

The M channel is a slowly activating and deactivating potassium channel that plays a critical role in the regulation of neuronal excitability. The M channel is formed by the association of the protein encoded by this gene and a related protein encoded by the KCNQ3 gene, both integral membrane proteins. M channel currents are inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. Defects in this gene are a cause of benign familial neonatal convulsions type 1 (BFNC), also known as epilepsy, benign neonatal type 1 (EBN1). At least five transcript variants encoding five different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

Kv7.2: Probably important in the regulation of neuronal excitability. Associates with KCNQ3 to form a potassium channel with essentially identical properties to the channel underlying the native M-current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs. KCNQ2/KCNQ3 current is blocked by linopirdine and XE991, and activated by the anticonvulsant retigabine. Muscarinic agonist oxotremorine-M strongly suppress KCNQ2/KCNQ3 current in cells in which cloned KCNQ2/KCNQ3 channels were coexpressed with M1 muscarinic receptors. Defects in KCNQ2 are the cause of benign familial neonatal seizures type 1 (BFNS1). A disorder characterized by clusters of seizures occurring in the first days of life. Most patients have spontaneous remission by 12 months of age and show normal psychomotor development. Some rare cases manifest an atypical severe phenotype associated with epileptic encephalopathy and psychomotor retardation. The disorder is distinguished from benign familial infantile seizures by an earlier age at onset. In some patients, neonatal convulsions are followed later in life by myokymia, a benign condition characterized by spontaneous involuntary contractions of skeletal muscles fiber groups that can be observed as vermiform movement of the overlying skin. Electromyography typically shows continuous motor unit activity with spontaneous oligo- and multiplet- discharges of high intraburst frequency (myokymic discharges). Some patients may have isolated myokymia. Defects in KCNQ2 are the cause of epileptic encephalopathy early infantile type 7 (EIEE7). EIEE7 is an autosomal dominant seizure disorder characterized by infantile onset of refractory seizures with resultant delayed neurologic development and persistent neurologic abnormalities. Belongs to the potassium channel family. KQT (TC 1.A.1.15) subfamily. Kv7.2/KCNQ2 sub-subfamily. 6 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral; Membrane protein, multi-pass; Channel, potassium

Chromosomal Location of Human Ortholog: 20q13.3

Cellular Component: voltage-gated potassium channel complex; plasma membrane; integral to membrane

Molecular Function: voltage-gated potassium channel activity; potassium channel activity; delayed rectifier potassium channel activity; ankyrin binding

Biological Process: synaptic transmission; nervous system development; axon guidance; transmission of nerve impulse; potassium ion transport

Disease: Seizures, Benign Familial Neonatal, 1; Epileptic Encephalopathy, Early Infantile, 7

1. Wuttke T.V., et al. (2008) J Physiol. 586(2): 545-555.

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