• Western blot analysis of lysates from Jurkat cells treated with EGF 200ng/ml 30', using IRF-3 (Phospho-Ser396) Antibody. The lane on the right is blocked with the phospho peptide.

Anti-Phospho-IRF3-Ser396 antibody (362-411 aa) (STJ90486)

SKU:
STJ90486

Current Stock:
Host: Rabbit
Applications: WB/IHC
Reactivity: Human/Mouse/Rat
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-Phospho-Interferon regulatory factor 3-Ser396 (362-411 aa) is suitable for use in Western Blot and Immunohistochemistry research applications.
Clonality: Polyclonal
Conjugation: Unconjugated
Isotype: IgG
Formulation: Liquid in PBS containing 50% Glycerol, 0.5% BSA and 0.02% Sodium Azide.
Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration: 1 mg/mL
Dilution Range: WB 1:500-2000
IHC-P 1:50-300
Storage Instruction: Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles.
Gene Symbol: IRF3
Gene ID: 3661
Uniprot ID: IRF3_HUMAN
Immunogen Region: 362-411 aa
Specificity: Phospho-IRF-3 (S396) Polyclonal Antibody detects endogenous levels of IRF-3 protein only when phosphorylated at S396.
Immunogen: The antiserum was produced against synthesized peptide derived from the human IRF-3 around the phosphorylation site of Ser396 at the amino acid range 362-411
Post Translational Modifications Constitutively phosphorylated on many Ser/Thr residues. Activated following phosphorylation by TBK1 and IKBKE. Innate adapter protein MAVS, STING1 or TICAM1 are first activated by viral RNA, cytosolic DNA, and bacterial lipopolysaccharide (LPS), respectively, leading to activation of the kinases TBK1 and IKBKE. These kinases then phosphorylate the adapter proteins on the pLxIS motif, leading to recruitment of IRF3, thereby licensing IRF3 for phosphorylation by TBK1. Phosphorylated IRF3 dissociates from the adapter proteins, dimerizes, and then enters the nucleus to induce IFNs. Ubiquitinated.ubiquitination involves RBCK1 leading to proteasomal degradation. Polyubiquitinated.ubiquitination involves TRIM21 leading to proteasomal degradation. Ubiquitinated by UBE3C, leading to its degradation. ISGylated by HERC5 resulting in sustained IRF3 activation and in the inhibition of IRF3 ubiquitination by disrupting PIN1 binding. The phosphorylation state of IRF3 does not alter ISGylation. Proteolytically cleaved by apoptotic caspases during apoptosis, leading to its inactivation. Cleavage by CASP3 during virus-induced apoptosis inactivates it, preventing cytokine overproduction. (Microbial infection) ISGylated. ISGylation is cleaved and removed by SARS-COV-2 nsp3 which attenuates type I interferon responses. (Microbial infection) Phosphorylation and subsequent activation of IRF3 is inhibited by vaccinia virus protein E3. (Microbial infection) Phosphorylated by herpes simplex virus 1/HHV-1 US3 at Ser-175 to prevent IRF3 activation.
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. 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. 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. 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. 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. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages. In response to Sendai virus infection, is recruited by TOMM70:HSP90AA1 to mitochondrion and forms an apoptosis complex TOMM70:HSP90AA1:IRF3:BAX inducing apoptosis. Key transcription factor regulating the IFN response during SARS-CoV-2 infection.
Protein Name Interferon Regulatory Factor 3
Irf-3
Database Links Reactome: R-HSA-1169408
Reactome: R-HSA-1606341
Reactome: R-HSA-168928
Reactome: R-HSA-3134973
Reactome: R-HSA-3134975
Reactome: R-HSA-3270619
Reactome: R-HSA-877300
Reactome: R-HSA-9013973
Reactome: R-HSA-909733
Reactome: R-HSA-918233
Reactome: R-HSA-933541
Reactome: R-HSA-936440
Reactome: R-HSA-936964
Reactome: R-HSA-9692916
Reactome: R-HSA-9705671
Cellular Localisation Cytoplasm
Nucleus
Mitochondrion
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
Alternative Antibody Names Anti-Interferon Regulatory Factor 3 antibody
Anti-Irf-3 antibody
Anti-IRF3 antibody

Information sourced from Uniprot.org

12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance