IRF-3 Antibody #4962
Inquiry Info. # 4962
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Supporting Data
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 52 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
IRF3 Antibody detects endogenous levels of total IRF3 protein.
Species Reactivity:
Human, Monkey
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthtic peptide corresponding to a residues surrounding proline 307 of human IRF-3. Antibodies are purified by protein A and peptide affinity chromatography.
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).
IRF3 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, IRF3 is present in the cytoplasm. Viral infection results in phosphorylation of IRF3, leading to its translocation to the nucleus, where it activates promoters containing IRF3-binding sites. Phosphorylation of IRF3 occurs at a cluster of serine and threonine residues in the carboxy-terminus between residues 385 and 405. This leads to an association with the p300/CBP coactivator and stimulation of DNA binding and transcriptional activity (5). During infection, IRF3 is likely activated through a pathway that includes activation of Toll-like receptors and of a kinase complex that includes IKKe and TBK1 (6,7).
IRF3 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, IRF3 is present in the cytoplasm. Viral infection results in phosphorylation of IRF3, leading to its translocation to the nucleus, where it activates promoters containing IRF3-binding sites. Phosphorylation of IRF3 occurs at a cluster of serine and threonine residues in the carboxy-terminus between residues 385 and 405. This leads to an association with the p300/CBP coactivator and stimulation of DNA binding and transcriptional activity (5). During infection, IRF3 is likely activated through a pathway that includes activation of Toll-like receptors and of a kinase complex that includes IKKe and TBK1 (6,7).
- 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.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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