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IRF-5 (E1N9G) Rabbit mAb #13496

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Inquiry Info. # 13496

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    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 60
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Immunocytochemistry) 1:400
    Flow Cytometry (Fixed/Permeabilized) 1:200

    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

    IRF-5 (E1N9G) Rabbit mAb recognizes endogenous levels of total IRF-5 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu169 of human IRF-5 protein.

    Background

    Interferon regulatory factors (IRFs) comprise a family of transcription factors that function within the Jak/Stat pathway to regulate interferon (IFN) and IFN-inducible gene expression in response to viral infection (1). IRFs play an important role in pathogen defense, autoimmunity, lymphocyte development, cell growth, and susceptibility to transformation. The IRF family includes nine members: IRF-1, IRF-2, IRF-9/ISGF3γ, IRF-3, IRF-4 (Pip/LSIRF/ICSAT), IRF-5, IRF-6, IRF-7, and IRF-8/ICSBP. All IRF proteins share homology in their amino-terminal DNA-binding domains. IRF family members regulate transcription through interactions with proteins that share similar DNA-binding motifs, such as IFN-stimulated response elements (ISRE), IFN consensus sequences (ICS), and IFN regulatory elements (IRF-E) (2).

    IRF-5 is expressed in lymphoid tissues and peripheral blood lymphocytes and participates in the induction of type I interferon genes following viral infection (3). Activation of IRF-5 signaling is triggered by components of the toll-like receptor (TLR) pathway, including TLR7 and MyD88 (4,5). Studies have shown that genetic variants of IRF-5 have been associated with disorders where the IFN pathway is abnormally activated, such as systemic lupus erythematosus (6,7).
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