The IRF3/IRF7, NF-κB, and AP-1 bind to PRD I/III, PRD II, and PRD IV, respectively, where they promote the transcription of IFN-α, IFN-β, and pro-inflammatory cytokines (TNF, IL6, IL1β, etc).. Following production, IFN-α and IFN-β mediate a positive feedback-production loop by binding to the IFN-α/β receptor (IFNAR) in an auto- and/or paracrine manner.
IFN-γ binding to the IFN-γR leads to STAT1 phosphorylation.
IFN-γ/receptor binding leads to subsequent endocytosis and IFN-γ nuclear localization sequence (NLS -guided biNLS -guidede IFN-γ-activated sequence (GAS) response element in the promoter region of IFN-γ-activated genes, such as IDO.
IFN-γ acts by binding to the heterodimeric IFN-γ receptor.
TTP inhibits TNF-alpha production from macrophages by destabilizing its mRNA through directly binding to the ARE of the TNF-alpha mRNA [17].
Gcs exert their effect by binding to the intracellular receptor, the glucocorticoid receptor alpha (GRα).
The 3a protein was found to induce serine phosphorylation within the IFN alpha-receptor subunit 1 (IFNAR1) degradation motif and to increase IFNAR1 ubiquitination.
However, TLR2 stimulation prior to IFN-γ decreased TBP binding to the CXCL11 promoter by 65%.
NK cells release IFN-γ after recognizing and binding to the target cells.
Alpha-MSH in the samples competed with 125I-labelled α-MSH in binding to the antibodies.
