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Mouse Irf3 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P70671 |
| Other Accession | Q764M6, Q4JF28, NP_058545.1 |
| Reactivity | Mouse |
| Predicted | Bovine, Pig |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 46852 Da |
| Antigen Region | 46-72 aa |
| Gene ID | 54131 |
|---|---|
| Other Names | Interferon regulatory factor 3, IRF-3, Irf3 |
| Target/Specificity | This Mouse Irf3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 46-72 amino acids from the N-terminal region of mouse Irf3. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Mouse Irf3 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Irf3 |
|---|---|
| Function | Key transcriptional regulator of type I interferon (IFN)- dependent immune responses which plays a critical role in the innate immune response against DNA and RNA viruses (PubMed:15800576). Regulates the transcription of type I IFN genes (IFN-alpha and IFN- beta) and IFN-stimulated genes (ISG) by binding to an interferon- stimulated response element (ISRE) in their promoters (PubMed:15800576). Acts as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical role in both the early and late phases of the IFNA/B gene induction (PubMed:16846591, PubMed:16979567, PubMed:20049431). Found in an inactive form in the cytoplasm of uninfected cells and following viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is phosphorylated by IKBKE and TBK1 kinases (PubMed:16846591, PubMed:16979567, PubMed:20049431). This induces a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes (PubMed:16846591, PubMed:16979567, PubMed:20049431). Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages (PubMed:16846591, PubMed:16979567, PubMed:20049431). |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:Q14653}. Nucleus {ECO:0000250|UniProtKB:Q14653}. Mitochondrion {ECO:0000250|UniProtKB:Q14653}. Note=Shuttles between cytoplasmic and nuclear compartments, with export being the prevailing effect. When activated, IRF3 interaction with CREBBP prevents its export to the cytoplasm. Recruited to mitochondria via TOMM70:HSP90AA1 upon Sendai virus infection. {ECO:0000250|UniProtKB:Q14653} |
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Provided below are standard protocols that you may find useful for product applications.
Background
Mediates interferon-stimulated response element (ISRE) promoter activation. Functions as a molecular switch for antiviral activity. DsRNA generated during the course of an viral infection leads to IRF3 phosphorylation on the C-terminal serine/threonine cluster. This induces a conformational change, leading to its dimerization, nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of genes under the control of ISRE. The complex binds to the IE and PRDIII regions on the IFN-alpha and IFN-beta promoters respectively. IRF-3 does not have any transcription activation domains (By similarity).
References
Marichal, T., et al. J. Allergy Clin. Immunol. 126(4):836-844(2010)
Menachery, V.D., et al. J. Virol. 84(19):9685-9694(2010)
Carrigan, S.O., et al. J. Immunol. 185(6):3602-3609(2010)
Wang, J., et al. J. Immunol. 185(3):1720-1729(2010)
Farlik, M., et al. Immunity 33(1):25-34(2010)
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