R Recombinant
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IRF-8 (D20D8) Rabbit mAb #5628
Filter:
- WB
- IP
- ChIP
Western blot analysis of extracts from Raji and Jurkat cells, untreated or treated with Human Interferon-α1 (hIFN-α1) #8927 (10 ng/ml; overnight) using IRF-8 (D20D8) Rabbit mAb.
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 50 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- Related Products
- Conjugates
Product Information
Product Usage Information
For optimal ChIP and ChIP-seq results, use 20 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 |
| Simple Western™ | 1:10 - 1:50 |
| Immunoprecipitation | 1:50 |
| Chromatin IP | 1:25 |
| Chromatin IP-seq | 1:25 |
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 (D20D8) Rabbit mAb detect endogenous levels of total IRF-8 protein. An unknown background band is detected at 80 kDa in some cell lines.
Species Reactivity:
Human, Mouse
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Rat, Monkey, Xenopus, Bovine
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly65 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
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
专品专有“专供研究使用”的专专或专似的专专声明， 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的， 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专，且专用于研专用途。将专品用于专断、专防或治专目的， 或专专售（专独或作专专成）或其他商专目的而专专专品，均需要 CST 的专独专可。客专：(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品，或使用专品制造任何商专专品，(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专，或使用专品开专任何与 CST 的专品或服专专争的专品或服专， (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专，(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品， (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专
For Research Use Only. Not For Use In Diagnostic Procedures.
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