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Render Timestamp: 2024-11-15T10:17:20.394Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-20 06:19:20.985
Product last modified at: 2024-09-13T07:01:40.942Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-IkappaB-alpha (Ser32) Antibody #9241

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Inquiry Info. # 9241

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    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY
    MW (kDa) 41
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    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-IkB-alpha (Ser32) Antibody detects endogenous levels of IkB-alpha only when phosphorylated at serine 32. The antibody does not recognize the corresponding phospho-serine of IkappaB-beta or IkappaB-epsilon.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Bovine, Dog, Pig

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Ser32 of human IkappaB-alpha. 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). Activation occurs via phosphorylation of IκBα at Ser32 and Ser36 followed by proteasome-mediated degradation that results in the release and nuclear translocation of active NF-κB (3-7). IκBα phosphorylation and resulting Rel-dependent transcription are activated by a highly diverse group of extracellular signals including inflammatory cytokines, growth factors, and chemokines. Kinases that phosphorylate IκB at these activating sites have been identified (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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