Kir2.1 Antibody (S112) [FITC]

Novus Biologicals | Catalog # NBP2-12900F

Novus Biologicals
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Key Product Details

Species Reactivity

Human, Mouse, Rat, Monkey

Applications

Immunohistochemistry, Immunocytochemistry/ Immunofluorescence, Microarray

Label

FITC (Excitation = 495 nm, Emission = 519 nm)

Antibody Source

Monoclonal Mouse IgG1 Clone # S112
View all Kir2.1 Primary Antibodies »

Product Specifications

Immunogen

Fusion protein amino acids 41-64 and 189-428 of mouse Kir2.1

Localization

Membrane

Specificity

Detects approx 45 kDa. No cross-reactivity against Kir2.2 or Kir2.3.

Clonality

Monoclonal

Host

Mouse

Isotype

IgG1

Applications for Kir2.1 Antibody (S112) [FITC]

Application
Recommended Usage

Immunocytochemistry/ Immunofluorescence

Optimal dilutions of this antibody should be experimentally determined.

Immunohistochemistry

Optimal dilutions of this antibody should be experimentally determined.

Microarray

Optimal dilutions of this antibody should be experimentally determined.
Application Notes
Optimal dilution of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Protein G purified

Formulation

PBS

Preservative

0.05% Sodium Azide

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C in the dark.

Background: Kir2.1

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.

Long Name

Inward Rectifier K(+) Channel Kir2.1

Alternate Names

ATFB9, HIRK1, IRK1, KCNJ2, LQT7, SQT3

Gene Symbol

KCNJ2

Additional Kir2.1 Products

Product Documents for Kir2.1 Antibody (S112) [FITC]

Certificate of Analysis

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Product Specific Notices for Kir2.1 Antibody (S112) [FITC]

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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Protocols

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FAQs

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