IRF-3 (D9J5Q) Mouse mAb #10949
- IHC
- IF
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 50-55 |
| Source/Isotype | Mouse IgG1 |
Application Key:
- IHC-Immunohistochemistry
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Immunohistochemistry (Paraffin) | 1:400 |
| Immunofluorescence (Immunocytochemistry) | 1:400 |
Storage
For a carrier free (BSA and azide free) version of this product see product #48932.
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
IRF-3 can inhibit cell growth and plays a critical role in controlling the expression of genes in the innate immune response (1-4). In unstimulated cells, IRF-3 is present in the cytoplasm. Viral infection results in phosphorylation of IRF-3 and leads to its translocation to the nucleus, where it activates promoters containing IRF-3-binding sites. Phosphorylation of IRF-3 occurs at a cluster of C-terminal Ser and Thr residues (between 385 and 405), leading to its association with the p300/CBP coactivator protein that promotes DNA binding and transcriptional activity (5). During infection, IRF-3 is likely activated through a pathway that includes activation of Toll-like receptors and a kinase complex that includes IKKε and TBK1 (6,7). IRF-3 is phosphorylated at Ser396 following viral infection, expression of viral nucleocapsid, and double-stranded RNA treatment. These events likely play a role in activation of IRF-3 (8).
- Taniguchi, T. et al. (2001) Annu Rev Immunol 19, 623-55.
- Honda, K. and Taniguchi, T. (2006) Nat Rev Immunol 6, 644-58.
- Hiscott, J. et al. (1999) J Interferon Cytokine Res 19, 1-13.
- Kim, T.Y. et al. (2003) J Biol Chem 278, 15272-8.
- Yoneyama, M. et al. (2002) J Interferon Cytokine Res 22, 73-6.
- Fitzgerald, K.A. et al. (2003) Nat Immunol 4, 491-6.
- Kopp, E. and Medzhitov, R. (2003) Curr Opin Immunol 15, 396-401.
- Servant, M.J. et al. (2003) J Biol Chem 278, 9441-7.
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