KCNJ2 antibody (Cytoplasmic Domain)

Catalog No. ABIN350394

Product Details anti-KCNJ2 Antibody

Target: KCNJ2 (Potassium Inwardly-Rectifying Channel, Subfamily J, Member 2 (KCNJ2))

Binding Specificity: Cytoplasmic Domain

Reactivity: Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This KCNJ2 antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (IHC)

Purpose: Rabbit antibody to KCNJ2

Specificity: Specific for KCNJ2.

Cross-Reactivity: Human, Mouse, Rat

Cross-Reactivity (Details): Other species not yet tested.

Purification: IgG

Immunogen: A synthetic peptide from the cytoplasmic domain of mouse KCNJ2 (HIRK1 IRK1 Kir2.1) conjugated to blue carrier protein was used as the antigen. The peptide is homologous in rat and human.

Isotype: IgG

Application Details

Application Notes: IHC WB. A concentration of 10-50 μg,ml is recommended. The optimal concentration should be determined by the end user. Not yet tested in other applications.

Restrictions: For Research Use only

Handling

Format: Lyophilized

Reconstitution: Reconstitute in 500 µL of sterile water. Centrifuge to remove any insoluble material.

Handling Advice: Avoid freeze and thaw cycles.

Storage: 4 °C,-20 °C

Storage Comment: Maintain the lyophilised/reconstituted antibodies frozen at -20C for long term storage and refrigerated at 2-8C for a shorter term. When reconstituting glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.

Expiry Date: 12 months

Target Details for KCNJ2

Target: KCNJ2 (Potassium Inwardly-Rectifying Channel, Subfamily J, Member 2 (KCNJ2))

Alternative Name: KCNJ2 (KCNJ2 Products)

Background: FUNCTION: 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. Can be blocked by extracellular barium or cesium. Tissue specificity: Heart brain placenta lung skeletal muscle and kidney. Diffusely distributed throughout the brain. Subcellular location: Membrane Multi-pass membrane protein. Involvement in disease: Defects in KCNJ2 are the cause of long QT syndrome type 7 (LQT7), also called Andersen syndrome or Andersen cardiodysrhythmic periodic paralysis. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to excercise or emotional stress. LQT7 manifests itself as a clinical triad consisting of potassium-sensitive periodic paralysis ventricular ectopy and dysmorphic features. Defects in KCNJ2 are the cause of short QT syndrome type 3 (SQT3). Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death. SQT3 has a unique ECG phenotype characterized by asymmetrical T waves.

UniProt: P35561