|Other Names||ATP-sensitive inward rectifier potassium channel 11, IKATP, Inward rectifier K(+) channel Kir62, Potassium channel, inwardly rectifying subfamily J member 11, KCNJ11|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP9209a was selected from the N-term region of human KCNJ11. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|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||This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium (By similarity). Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation.|
|Cellular Location||Membrane; Multi-pass membrane protein.|
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ATP-sensitive potassium (K(ATP)) channels are found in endocrine cells, neurons and both smooth and striated muscle, where they play an important role in controlling insulin secretion and vascular tone, and protect neurons under metabolic stress. Kir6.2 is a member of the inward rectifier potassium channel family, which is characterised by a greater tendency to allow potassium flow into the cell rather than out of it. It associates with the sulphonylurea receptor SUR1/ABCC8 to form a subfamily of K(ATP) channels that, when mutated or misregulated, are associated with forms of hyperinsulinemic hypoglycemia, neonatal diabetes, or pre-disposition to type 2 diabetes mellitus.
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