Render Target: STATIC
Render Timestamp: 2024-12-02T11:50:10.899Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-08-01 15:25:48.375
Product last modified at: 2024-11-22T16:30:08.517Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-IKKγ (Ser376) Antibody #2689

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 50
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-IKKγ (Ser376) Antibody detects endogenous levels of IKKγ protein only when phosphorylated at Ser376.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser376 of human IKKγ protein. Antibodies are purified by protein A and peptide affinity chromatography.

    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 mouse, mutation of the orthologous residue (Ser369) to alanine leads to enhanced IKKγ-mediated stimulation of IKKβ kinase activity (15).
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