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Render Timestamp: 2024-07-26T10:38:18.422Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

IKKγ (DA10-12) Mouse mAb #2695

Filter:
  • WB

    Supporting Data

    REACTIVITY H R
    SENSITIVITY Endogenous
    MW (kDa) 50
    Source/Isotype Mouse IgG1
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    IKKγ (DA10-12) Mouse mAb detects endogenous levels of total IKKγ protein.


    Species Reactivity:

    Human, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with full length human GST-IKKγ protein.

    Background

    The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).
    Activation of the NF-κB pathway by the T-cell lymphotrophic virus Tax protein or by TNF-α treatment leads to IKKβ-dependent phosphorylation of human IKKγ, primarily at Ser376 (14). In mice, mutation of the orthologous residue (Ser369) to alanine leads to enhanced IKKγ-mediated stimlulation of IKKβ kinase activity (15).

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