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Kir2.1 Antibody (S112) [DyLight 594]

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Product Details

Summary
Reactivity Hu, Mu, Rt, PmSpecies Glossary
Applications Simple Western, ICC/IF, IHC, MA
Clone
S112
Clonality
Monoclonal
Host
Mouse
Conjugate
DyLight 594

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Kir2.1 Antibody (S112) [DyLight 594] Summary

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.
Isotype
IgG1
Clonality
Monoclonal
Host
Mouse
Gene
KCNJ2
Purity
Protein G purified
Innovator's Reward
Test in a species/application not listed above to receive a full credit towards a future purchase.

Applications/Dilutions

Dilutions
  • Immunocytochemistry/ Immunofluorescence
  • Immunohistochemistry
  • Microarray
  • Simple Western
Application Notes
Optimal dilution of this antibody should be experimentally determined.

Packaging, Storage & Formulations

Storage
Store at 4C in the dark.
Buffer
50mM Sodium Borate
Preservative
0.05% Sodium Azide
Purity
Protein G purified

Notes



DyLight (R) is a trademark of Thermo Fisher Scientific Inc. and its subsidiaries.

Alternate Names for Kir2.1 Antibody (S112) [DyLight 594]

  • ATFB9
  • Cardiac inward rectifier potassium channel
  • HHBIRK1
  • HHIRK1
  • HIRK1
  • Inward rectifier K(+) channel Kir2.1
  • inward rectifier K+ channel KIR2.1
  • inward rectifier potassium channel 2
  • IRK1
  • IRK-1
  • IRK1LQT7
  • KCNJ2
  • Kir2.1
  • LQT7
  • Potassium channel, inwardly rectifying subfamily J member 2
  • potassium inwardly-rectifying channel, subfamily J, member 2
  • SQT3

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.

Limitations

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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Product General Protocols

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Video Protocols

ICC/IF Video Protocol

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Secondary Antibodies

 

Isotype Controls

Additional Kir2.1 Products

Array NBP2-12900DL594

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Bioinformatics

Gene Symbol KCNJ2