IRF-8 (E6J8Q) XP® Rabbit mAb (PE Conjugate) #96564
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
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.
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