Render Target: SSR
Render Timestamp: 2024-12-19T21:19:03.974Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-12-17 23:02:08.237
Product last modified at: 2024-12-18T09:00:10.948Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

IκBα (L27H11) Mouse mAb (BSA and Azide Free) #90155

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Mouse IgG1
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

    BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    Storage

    Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    Specificity / Sensitivity

    IκBα (L27H11) Mouse mAb (BSA and Azide Free) detects endogenous levels of total IκBα protein.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a fragment corresponding to the amino terminus of human IκBα.

    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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