|Positive WB detected in||A549 cells|
|Positive IHC detected in||human brain tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:200-1:1000|
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
19965-1-AP targets Kir2.1 in WB, IHC, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||mouse, rat, rabbit|
|Host / Isotype||Rabbit / IgG|
|Full Name||potassium inwardly-rectifying channel, subfamily J, member 2|
|Calculated molecular weight||48 kDa|
|Observed molecular weight||50 kDa, 60 kDa|
|GenBank accession number||NM_000891|
|Gene ID (NCBI)||3759|
|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.|
KCNJ2, also named as HHBIRK1, HHIRK1, IRK1, KIR2.1, LQT7 and SQT3, belongs to the inward rectifier-type potassium channel family. KCNJ2 probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. 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. KCNJ2 can be blocked by extracellular barium or cesium. Defects in KCNJ2 are the cause of long QT syndrome type 7 (LQT7). Defects in KCNJ2 are the cause of short QT syndrome type 3 (SQT3). The antibody recognizes the C-term of KCNJ2.
Kir2.1-mediated membrane potential promotes nutrient acquisition and inflammation through regulation of nutrient transporters.
J Mol Cell Cardiol
Altered long non-coding RNA expression profile in rabbit atria with atrial fibrillation: TCONS_00075467 modulates atrial electrical remodeling by sponging miR-328 to regulate CACNA1C.
J Cell Mol Med
Long noncoding RNA TCONS-00106987 promotes atrial electrical remodelling during atrial fibrillation by sponging miR-26 to regulate KCNJ2.
J Cell Mol Med
Nucleoporin 107 facilitates the nuclear export of Scn5a mRNA to regulate cardiac bioelectricity.