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STAT1 — TLR3

Text-mined interactions from Literome

Heinz et al., J Biol Chem 2003 : In murine macrophages, IFN-beta induced TLR3 up-regulation required IFNAR1, STAT1 , and in part IRF-1, but not the Janus kinase ( Jak ) family member Tyk2
Rhee et al., J Biol Chem 2003 : TLR induced phosphorylation of Ser-727 STAT1 could be blocked by the selective p38 mitogen activated protein kinase inhibitor SB203580 ... Lastly, TLR4 induced activation of Ser-727 STAT1 phosphorylation could be blocked by rottlerin, a specific inhibitor of protein kinase C-delta
Punturieri et al., J Immunol 2004 : Specific engagement of TLR4 or TLR3 does not lead to IFN-beta mediated innate signal amplification and STAT1 phosphorylation in resident murine alveolar macrophages
Shoenfelt et al., J Endotoxin Res 2006 : Unlike other cell types, the p38 mitogen activated protein kinase was necessary, but not sufficient, for TLR induced phosphorylation of Ser-727 STAT1 in macrophages
Elco et al., J Interferon Cytokine Res 2007 (Fibrosarcoma) : Although U3A cells are deficient in Stat1, we found that Stat1 was not required for basal TLR3 expression because other cell lines lacking Stat1 expressed TLR3
Rothlin et al., Cell 2007 (Inflammation) : TLR induction of IFNAR-STAT1 signaling upregulates the TAM system, which in turn usurps the IFNAR-STAT1 cassette to induce the cytokine and TLR suppressors SOCS1 and SOCS3
Homma et al., Int Arch Allergy Immunol 2010 : Cooperative activation of CCL5 expression by TLR3 and tumor necrosis factor-alpha or interferon-gamma through nuclear factor-kappaB or STAT-1 in airway epithelial cells
Bhattacharyya et al., Proc Natl Acad Sci U S A 2011 : Inhibition of TLR3 mediated STAT1 activation occurs via two mechanisms, impairment of type I IFN secretion and induction of SOCS1
Tel et al., Cancer Immunol Immunother 2012 : Furthermore, oxaliplatin decreased TLR induced STAT1 and STAT3 expression, and NF-?B mediated responses
Yang et al., J Immunol 2013 (Inflammation) : TLR3 induced activation of STAT1 contributed to the generation of inflammatory mediators, which was significantly attenuated in NOX2- and p47(phox)-deficient macrophages, suggesting a role for ROS-STAT1 in TLR3 mediated innate immune responses