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NFκB p65 (Total/Phospho) ELISA kit

 
ADI-EKS-446A 96 wells 579.00 USD
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Replaces Prod. #: ADI-EKS-446

  • Fast- measure the active form of NFκB p65 in just 1.5 hours
  • Higher throughput - 96 well plate based method faster than EMSA and Western blot
  • Sensitive - colorimetric detection
The NFκB p65 EIA kit provides a sensitive, rapid and reliable method to measure the active form of NFκB p65. The assay uses streptavidin-coated plates with bound NFκB biotinylated-consensus sequence to capture only the active form of NFκB. The captured active NFκB is incubated with a specific NFκB p65 antibody, which is then detected using an HRP conjugated secondary antibody. The assay is developed with a chemiluminescent substrate and the signal is detected using a luminometer. Higher throughput 96 well plate based method faster than EMSA and Western blot with sensitive chemiluminescent detection.

Product Specification

Assay Time:1.5 hours
 
Applications:ELISA
 
Application Notes:For the quantitative determination of active NFκB p65 in cell lysates of human, mouse, and rat origin.
 
Species reactivity:Human, Mouse, Rat
 
Use/Stability:Reagents require separate storage conditions upon receipt.
 
Shipping:Shipped on Dry Ice
 
Short Term Storage:+4°C
 
Kit/Set Contains:Microtiter plate, cell lysis buffer, 10X wash buffer, detection reagent, stop solution, plate sealer, capture antibody, detector antibody, positive control lysate
 
Scientific Background:Stimulation of the canonical NFκB pathway leads to the phosphorylation of and subsequent degradation of IκB; phosphorylation of the latter is controlled by a specific set of proteins referred to as the I Kappa Kinases (IKK), which include IKKα and IKKβ. Under normal conditions, IκB acts as a key regulatory molecule in that it sequesters p65 or Rel A within the cytoplasm; this blocks NFκB dependent transcription. Upon phosphorylation of IκB by IKK’s, p65 is released and free to associate with the p50 subunit; p65 acts as a transactivator whereas p50 possesses DNA binding activity. Complex formation leads to the subsequent translocation of the NFκB complex into the nucleus and the concomitant up-regulation of NFκB dependent genes. Disruption of this signaling nexus has been documented in a number of human pathological conditions including inflammation, infection and cancer.
 

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