◀ Back to TLR9
IRF7 — TLR9
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
IRF7
→
TLR9
(increases, TLR9 Activity, IRF7 Activity)
Evidence: Thus, inhibition of mTOR signaling during pDC activation through TLR9 blocks the interaction between TLR9 and MyD88 and the subsequent phosphorylation and nuclear translocation of IRF7, resulting in impaired IFN?/? production72 (FIG. 2D).
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Reactome Reaction:
IRF7
→
TLR9
(reaction)
Marié et al., Mol Cell Biol 2000*, Kawai et al., Nat Immunol 2004, Honda et al., Proc Natl Acad Sci U S A 2004*, Uematsu et al., J Exp Med 2005, Ning et al., Mol Cell Biol 2008
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Reactome Reaction:
IRF7
→
TLR9
(indirect_complex)
Kawai et al., Nat Immunol 2004, Honda et al., Proc Natl Acad Sci U S A 2004*, Uematsu et al., J Exp Med 2005, Ning et al., Mol Cell Biol 2008
Text-mined interactions from Literome
Guo et al., J Immunol 2005
:
This study illustrates the crucial
roles for AP-1,
IRF-1 , IRF-2, and STAT1 in the regulation of murine
TLR9 expression
Guiducci et al., J Exp Med 2008
:
PI3K is critical for the nuclear translocation of
IRF-7 and type I IFN production by human plasmacytoid predendritic cells in
response to
TLR activation
Atzei et al., J Biol Chem 2010
:
We now describe the first functional characterization of the human ortholog of Cactin ( hCactin ) and show that it acts as a negative regulator of TLRs. Overexpression of hCactin suppresses
TLR induced
activation of NF-?B and
interferon-regulatory factor transcription factors and induction of TLR-responsive genes, whereas knockdown of endogenous hCactin augments TLR induction of these responses
Sisirak et al., Int J Cancer 2013
(Breast Neoplasms) :
Mechanisms of type I IFN inhibition did not involve
TLR downregulation but the
inhibition of
IRF-7 expression and nuclear translocation in pDC after their exposure to tumor derived supernatants or recombinant TGF-ß1 and TNF-a