R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
IRF-8 (E6J8Q) XP® Rabbit mAb #83413
Filter:
- WB
- IP
- IHC
- F
- ChIP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 50 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- F-Flow Cytometry
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
For optimal ChIP results, use 10 μl of antibody and 10 μg of chromatin (approximately 4 × 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
| Immunoprecipitation | 1:100 |
| IHC Leica Bond | 1:250 - 1:1000 |
| Immunohistochemistry (Paraffin) | 1:250 - 1:1000 |
| Flow Cytometry (Fixed/Permeabilized) | 1:400 - 1:1600 |
| 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.
For a carrier-free (BSA and azide free) version of this product see product #28852.
For a carrier-free (BSA and azide free) version of this product see product #28852.
Protocol
Specificity / Sensitivity
IRF-8 (E6J8Q) XP® Rabbit mAb recognizes endogenous levels of total IRF-8 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human 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/ICSBP is expressed predominately 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). Expression of IRF-8 can lead to the 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 and impaired production of interferons, as well as deregulated hematopoiesis that resembles chronic myelogenous leukemia (7,8). IRF-8 also regulates bone metabolism by suppressing osteoclast formation (9).
IRF-8/ICSBP is expressed predominately 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). Expression of IRF-8 can lead to the 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 and impaired production of interferons, as well as deregulated hematopoiesis that resembles chronic myelogenous leukemia (7,8). IRF-8 also regulates bone metabolism by suppressing osteoclast formation (9).
- Taniguchi, T. et al. (2001) Annu Rev Immunol 19, 623-55.
- Honda, K. and Taniguchi, T. (2006) Nat Rev Immunol 6, 644-58.
- Driggers, P.H. et al. (1990) Proc Natl Acad Sci U S A 87, 3743-7.
- Weisz, A. et al. (1992) J Biol Chem 267, 25589-96.
- Burchert, A. et al. (2004) Blood 103, 3480-9.
- Lehtonen, A. et al. (2003) Cytokine 24, 81-90.
- Holtschke, T. et al. (1996) Cell 87, 307-17.
- Fehr, T. et al. (1997) J Exp Med 185, 921-31.
- Zhao, B. et al. (2009) Nat Med 15, 1066-71.
限制使用
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