IRF family of transcription factors as regulators of host defense.

By Tadatsugu Taniguchi, K. Ogasawara, and Akinori Takaoka, N. Tanaka. Annual Review of Immunology, 2001

1,729 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/7b28bc9022d936f0ee025e5b38219899ee534cbd

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Citations in the corpus

IRFs: master regulators of signalling by Toll-like receptors and cytosolic pattern-recognition receptors (2006, neutral): “The mammalian IRF family comprises nine members: IRF1 , IRF2 , IRF3 , IRF4 (also known as LSIRF, PIP or ICSAT), IRF5 , IRF6 , IRF7 , IRF8 (also known as ICSBP) and IRF9 (also known as ISGF3γ”
TICAM-1, an adaptor molecule that participates in Toll-like receptor 3–mediated interferon-β induction (2003, background): “AP-1 and IRF-3 activation by TICAM-1 NF-κB, AP-1 and interferon-regulatory factor (IRF)-3 function as transcription factors for IFN-β activatio”
Integral role of IRF-5 in the gene induction programme activated by Toll-like receptors (2005, background): “The IRF family of transcription factors has gained much attention for its contribution to the regulation of the immune syste”
Plasmacytoid dendritic cells in immunity (2004, background): “Transcriptional regulation of IFN-β and IFN-α genes is controlled mainly by IRF3 and/or IRF7 (ref”
Toll-like receptor signalling (2004, background): “The IRFs are a family of transcription factors that are involved both in the induction of type I IFNs and in the response to IFN”
Toll-like receptors. (2003, background): “IRF The IRF family of transcription factors is composed of nine members that are critical regulators of innate immune responses (247).”
RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β (2002, background): “IFN-β (as well as IFN-α) elicits cellular responses through activation/induction of transcription factors, which include ISGF3 (a heterotrimeric complex consisting of Stat1, Stat2 and interferon regulatory factor 9 (IRF-9)), GAF/AAF (the Stat1 homodimer) and IRF-1 (ref”
Latent enhancers activated by stimulation in differentiated cells. (2013, neutral): “, 1999) binding occurs at IRF-type binding sites formed by direct repeats of 50-GAAA-30 units (Taniguchi et al., 2001).”
Identification and characterization of enhancers controlling the inflammatory gene expression program in macrophages. (2010, background): “…inflammatory gene expression, an obvious prediction is that they should be enriched for binding sites for stimulus-activated TFs required for the deployment of the inflammatory gene expression program, like NF-kB (Rel) and IRF family members (Taniguchi et al., 2001; Hayden and Ghosh, 2008).”
Lipopolysaccharide signaling in endothelial cells (2006, background): “112 IRF3 is a member of a family of transcription factors that are involved in the induction of type I IFNs that translocate to the nucleus upon phosphorylation and dimerization”
Interferon signalling network in innate defence (2006, background): “IRF-2 is constitutively expressed in most cell types, and functions as an attenuator at the ISRE to suppress ISGF3-mediated signalling (Taniguchi et al., 2001; Taki, 2002).”
Mutations in IRF6 cause Van der Woude and popliteal pterygium syndromes (2002, background): “Most IRFs regulate the expression of interferon-α and -β after viral infectio”