How is IRF1 activated?
IRF1 both modulates and is regulated by activating and repressive epigenetic marks on chromatin, including histone methylation (such as H3K4me3 and H3K27me3) or acetylation at promoter proximal sites. IRF1 can also act cooperatively with other transcription factors to induce gene expression.
What does IRF1 do?
IRF-1 has been shown to play roles in the immune response, regulating apoptosis, DNA damage and tumor suppression.
What activates IRF7?
IRF7 is activated by pathogenic nuclei acids through pathways mediated by TLR3, -7 and -9, RIG-I and likely DNA-dependent activator of IRF and IFI16, as well as by TLR2-mediated signaling pathway.
How does NF-ΚB induce gene expression?
How does NF-κB induce gene expression? A small, hydrophobic ligand binds to NF-κB, activating it. Phosphorylation of the inhibitor Iκ-B dissociates the complex between it and NF-κB, and allows NF-κB to enter the nucleus and stimulate transcription.
Is STAT3 a transcription factor?
STAT3 belongs to the signal transducer and activator of transcription (STAT) family of signal responsive transcription factors which consists of seven members encoded by distinct genes.
What is interferon immunity?
Interferons are proteins that are part of your natural defenses. They tell your immune system that germs or cancer cells are in your body. And they trigger killer immune cells to fight those invaders. Interferons got their name because they “interfere” with viruses and keep them from multiplying.
Is IRF a transcription factor?
Interferon regulatory factors (IRFs) are a family of transcription factors that regulate many aspects of innate and adaptive immune responses—including driving anti-viral responses, responding to pathogens to drive pro-inflammatory responses and regulating immune cell differentiation (1).
Is IRF7 an ISG?
While IRF-3 is constitutively expressed in many tissues, IRF-7 is an ISG required for the expression of most IFN-α subtypes, and thus a key mediator of the type I IFN amplification loop [2], [9], [10].
What genes does NF kB regulate?
NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells.
How does IΚB phosphorylation lead to NF-κB activation and transcription?
Phosphorylation of serine residues in the signal responsive region (SRR) of classical IκBs by IKKβ leads to IκB ubiquitination and subsequent proteosomal degradation. This results in release of the NF-κB dimer, which can then translocate to the nucleus and induce transcription of target genes.
What is a STAT3 mutation?
STAT3 loss- of-function mutations are responsible for hyper- immunoglobulin E syndrome, also called Job’s syndrome, which is characterized by recurrent skin infections, unusual eczema-like skin rashes, and susceptibility to severe lung infections.
How is STAT3 phosphorylated?
Function. STAT3 is a member of the STAT protein family. In response to cytokines and growth factors, STAT3 is phosphorylated by receptor-associated Janus kinases (JAK), forms homo- or heterodimers, and translocates to the cell nucleus where it acts as a transcription activator.
How does Sting stimulate phosphorylation of IRF3?
Here, we showed that STING stimulates phosphorylation of IRF3 by the kinase TBK1 (TANK-binding kinase 1) in an in vitro reconstitution system. With this system, we identified a carboxyl-terminal region of STING that was both necessary and sufficient to activate TBK1 and stimulate the phosphorylation of IRF3.
What is the kinase that activates IRF3 and IRF7?
Induction of interferon-alpha (IFNalpha) gene expression in virus-infected cells requires phosphorylation-induced activation of the transcription factors IRF3 and IRF7. However, the kinase (s) that targets these proteins has not been identified.
Which kinases are responsible for IRF phosphorylation in Newcastle disease virus?
Using a combined pharmacological and genetic approach, we found that none of the kinases tested was responsible for IRF phosphorylation in cells infected with Newcastle disease virus (NDV).