Render Target: STATIC
Render Timestamp: 2024-12-06T11:44:59.249Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-09-30 01:56:27.549
Product last modified at: 2024-09-30T08:01:39.204Z
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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.

IκB-ζ (D4I7C) Rabbit mAb #76041

Filter:
  • WB
  • IP
  • ChIP

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa) 75, 85
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • ChIP-Chromatin Immunoprecipitation 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    For optimal ChIP results, use 10 μl of antibody and 10 μg of chromatin (approximately 4 x 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Chromatin IP 1:50

    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

    IκB-ζ (D4I7C) Rabbit mAb recognizes endogenous levels of total mouse IκB-ζ protein. This antibody has weak reactivity for rat and human. Product #93726 is preferred for western blot.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly108 of mouse IκB-ζ 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). 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).
    IκB-ζ (MAIL, INAP) is a unique IκB family member homologous to Bcl-3 and induced by IL-1 and Toll-like receptor (TLR) ligands (9-11). Like other family members, it contains carboxyl terminal ankyrin-repeats responsible for interaction with NF-κB, particularly p50. Unlike classical IκB family members (α, β, ε) which inhibit NF-κB translocation and are rapidly degraded upon cytokine treatment, IκB-ζ is cytokine-inducible and localized to the nucleus where it regulates NF-κB DNA binding and transactivation (12-14). Induction of IκB-ζ is required for TLR/IL-1 induction of a subset of NF-κB target genes, including IL-6 (15). However, the IκB-ζ can also inhibit transactivation of other targets, such as TNF-α (14,15).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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