|Other Names||Potassium voltage-gated channel subfamily KQT member 3, KQT-like 3, Potassium channel subunit alpha KvLQT3, Voltage-gated potassium channel subunit Kv73, KCNQ3|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Probably important in the regulation of neuronal excitability. Associates with KCNQ2 or KCNQ5 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.|
|Cellular Location||Membrane; Multi-pass membrane protein.|
|Tissue Location||Predominantly expressed in brain.|
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The M channel is a slowly activating and deactivatingpotassium channel that plays a critical role in the regulation ofneuronal excitability. The M channel is formed by the associationof the protein encoded by this gene and one of two related proteinsencoded by the KCNQ2 and KCNQ5 genes, both integral membraneproteins. M channel currents are inhibited by M1 muscarinicacetylcholine receptors and activated by retigabine, a novelanti-convulsant drug. Defects in this gene are a cause of benignfamilial neonatal convulsions type 2 (BFNC2), also known asepilepsy, benign neonatal type 2 (EBN2).
Bailey, S.D., et al. Diabetes Care (2010) In press :Gomez-Posada, J.C., et al. J. Neurosci. 30(27):9316-9323(2010)Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :Talmud, P.J., et al. Am. J. Hum. Genet. 85(5):628-642(2009)Hahn, A., et al. Brain Dev. 31(7):515-520(2009)
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