|Positive WB detected in||rat heart tissue, HepG2 cells, human heart tissue, rat skeletal muscle tissue|
|Western Blot (WB)||WB : 1:200-1:1000|
|Sample-dependent, check data in validation data gallery|
16920-1-AP targets Kir6.2 in WB, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Kir6.2 fusion protein Ag10262|
|Full Name||potassium inwardly-rectifying channel, subfamily J, member 11|
|Calculated molecular weight||390 aa, 44 kDa|
|Observed molecular weight||48 kDa|
|GenBank accession number||BC064497|
|Gene ID (NCBI)||3767|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
Kir6.2 (also known as BIR or IKATP), encoded by the KCNJ11 gene, is the pore-forming unit of the ATP-sensitive K+ channel, an inward-rectifier potassium ion channel. Kir6.2 is controlled by G-proteins and is found associated with the sulfonylurea receptor (SUR) to constitute the ATP-sensitive K+ channel. The KCNJ11 gene is located at 11p15.1 and has no intron. Mutations in KCNJ11 are a cause of familial PHHI, an autosomal recessive disorder characterized by unregulated ins secretion. Defects in KCNJ11 may also contribute to autosomal dominant non-ins-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM).