|Application ||WB, IHC, E|
|Other Accession||NP_000516, 3767|
|Calculated MW||43541 Da|
|Other Names||ATP-sensitive inward rectifier potassium channel 11, IKATP, Inward rectifier K(+) channel Kir6.2, Potassium channel, inwardly rectifying subfamily J member 11, KCNJ11|
|Format||0.5 mg IgG/ml in Tris saline (20mM Tris pH7.3, 150mM NaCl), 0.02% sodium azide, with 0.5% bovine serum albumin|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Goat Anti-KCNJ11 / KATP / Antibody is for research use only and 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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Provided below are standard protocols that you may find useful for product applications.
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins and is found associated with the sulfonylurea receptor SUR. Mutations in this gene are a cause of familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion. Defects in this gene may also contribute to autosomal dominant non-insulin-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM). Multiple alternatively spliced transcript variants that encode different protein isoforms have been described for this gene.
Glycemia determines the effect of type 2 diabetes risk genes on insulin secretion. Heni M, et al. Diabetes, 2010 Aug 29. PMID 20802253.
COMMON VARIANTS IN 40 GENES ASSESSED FOR DIABETES INCIDENCE AND RESPONSE TO METFORMIN AND LIFESTYLE INTERVENTIONS IN THE DIABETES PREVENTION PROGRAM. Jablonski KA, et al. Diabetes, 2010 Aug 3. PMID 20682687.
Variation at the NFATC2 Locus Increases the Risk of Thiazolinedinedione-Induced Edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) Study. Bailey SD, et al. Diabetes Care, 2010 Jul 13. PMID 20628086.
Coronary artery calcification and its relationship to validated genetic variants for diabetes mellitus assessed in the Heinz Nixdorf recall cohort. Pechlivanis S, et al. Arterioscler Thromb Vasc Biol, 2010 Sep. PMID 20616309.
A validation study of type 2 diabetes-related variants of the TCF7L2, HHEX, KCNJ11, and ADIPOQ genes in one endogamous ethnic group of north India. Gupta V, et al. Ann Hum Genet, 2010 Jul. PMID 20597906.
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