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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

LITAF (F3W1P) Rabbit mAb #41610

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  • WB
  • IP

    Product Specifications

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 23, 20
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 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

    LITAF (F3W1P) Rabbit mAb recognizes endogenous levels of total LITAF protein. This antibody recognizes both isoforms of mouse LITAF and detects a 90 kDa protein of unknown identity in some cell lines.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro58 of human LITAF protein.

    Background

    Lipopolysaccharide-induced TNF factor (LITAF), also known as PIG7 and SIMPLE, is a protein that contributes to the regulation of the inflammatory cytokine TNF-α (1-3). LITAF was identified as a transcription factor involved in LPS-induced TNF-α expression through interaction with the TNF-α promoter (1,4). The same protein, called PIG7, was independently described in a model for p53 regulation (2). A putative alternative spliced form of LITAF, named SIMPLE, encodes a protein with a unique carboxyl terminus (3). Studies on LITAF-deficient mice demonstrate that LITAF plays a significant role in the regulation of several inflammatory cytokines in response to LPS (5). LITAF regulation can occur through phosphorylation by p38α via the TLR pathway that leads to its nuclear translocation (5). Mutation in the LITAF/SIMPLE gene has been associated with an autosomal dominant demyelinating form of Charcot-Marie-Tooth disease (6).
    For Research Use Only. Not for Use in Diagnostic Procedures.
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