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Interferon regulatory factors (IRF) are proteins which regulate transcription of interferons (see regulation of gene expression). [1] Interferon regulatory factors contain a conserved N-terminal region of about 120 amino acids, which folds into a structure that binds specifically to the IRF-element (IRF-E) motifs, which is located upstream of the interferon genes. [2]
[[Category:Signaling pathway templates]] to the <includeonly> section at the bottom of that page. Otherwise, add <noinclude>[[Category:Signaling pathway templates]]</noinclude> to the end of the template code, making sure it starts on the same line as the code's last character.
IRF3 is a member of the interferon regulatory transcription factor (IRF) family. [5] IRF3 was originally discovered as a homolog of IRF1 and IRF2.IRF3 has been further characterized and shown to contain several functional domains including a nuclear export signal, a DNA-binding domain, a C-terminal IRF association domain and several regulatory phosphorylation sites. [6]
Interferon regulatory factor 8 (IRF8) also known as interferon consensus sequence-binding protein (ICSBP), is a protein that in humans is encoded by the IRF8 gene. [5] [6] [7] IRF8 is a transcription factor that plays critical roles in the regulation of lineage commitment and in myeloid cell maturation including the decision for a common myeloid progenitor (CMP) to differentiate into a ...
IRF5 is a direct transducer to interferon signaling and is activated via phosphorylation. [11] The IRF family can also initiate the JAK/STAT signaling pathway by binding to transmembrane receptors that activate JAK. [12] IRFs, IFNs, and the JAK/STAT signaling pathway work together to fight viral infections in mammals through specific signals. [13]
After recognizing viral DNA, DNA sensors initiate the downstream signaling pathways by activating STING-mediated interferon response. [15] Adenovirus, herpes simplex virus, HSV-1 and HSV-2, as well as the negative-stranded RNA virus, vesicular stomatitis virus (VSV), have been shown to be able to activate a STING-dependent innate immune ...
[27] [28] Reducing IFN-α activity may prevent signaling via STAT1, STAT2, or IRF9 (as with JEV infection) or through the JAK-STAT pathway (as with DEN-2 infection). [26] Several poxviruses encode soluble IFN receptor homologs—like the B18R protein of the vaccinia virus—that bind to and prevent IFN interacting with its cellular receptor ...
The upstream signaling pathway is triggered by the binding of a signaling molecule, a ligand, to a receiving molecule, a receptor. Receptors and ligands exist in many different forms, and only recognize/bond to particular molecules. Upstream extracellular signaling transduce a variety of intracellular cascades. [1]
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