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IRF-8 (F7M3K) Rabbit mAb #32303

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  • WB
  • IP
  • IHC

    Supporting Data

    REACTIVITY M R
    SENSITIVITY Endogenous
    MW (kDa) 50
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200
    Immunohistochemistry (Paraffin) 1:200 - 1:800

    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-8 (F7M3K) Rabbit mAb recognizes endogenous levels of total IRF-8 protein. Non-specific staining was observed in liver by immunohistochemistry. 

    Species Reactivity:

    Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of mouse IRF-8 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-8/ICSCP is expressed predominantly in hematopoietic cells and is further increased upon treatment with interferon (3,4). IRF-8 can function as a transcription repressor of ICS-containing promoters (4). IRF-8 expression can lead to downregulation of the anti-apoptotic protein Bcl-2 (5). Originally described as being induced by IFN-γ, IRF-8 expression is also elevated by IRF-α as well as IL-12 in NK and T cells (6). IRF-8 deficient mice have enhanced susceptibility to various pathogens, impaired interferon production, and deregulated hematopoiesis resembling chronic myelogenous leukemia (7,8). IRF-8 also regulates bone metabolism by suppressing osteoclast formation (9).
    For Research Use Only. Not for Use in Diagnostic Procedures.
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