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EPHB2 — TLR9

Text-mined interactions from Literome

An et al., Immunology 2002 : Involvement of ERK , p38 and NF-kappaB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cells
Goral et al., J Immunol 2005 (Inflammation) : Acute ethanol treatment inhibited IL-6 and TNF-alpha synthesis and impaired p38 and ERK1/2 activation induced by TLR2, TLR4, and TLR9 ligands
Miller et al., Arterioscler Thromb Vasc Biol 2005 (Atherosclerosis) : In turn, TLR4 regulated phosphorylation of ERK1/2 but not of Akt, suggesting that mmLDL induced PI3K activation is TLR4 independent
Amcheslavsky et al., J Cell Physiol 2006 : Since both RANKL-RANK and CpG-ODN-TLR9 interactions result in NF-kappaB activation, p38 and ERK phosphorylation, and TNF-alpha synthesis ( all implicated in osteoclastogenesis ), we hypothesized that CpG-ODN ( but not RANKL ) in addition induces the synthesis of an anti-osteoclastogenic factor
Banerjee et al., Proc Natl Acad Sci U S A 2006 : Despite rescuing TLR dependent ERK activation in nfkb1 ( -/- ) bone marrow derived macrophages by using an estrogen receptor regulated version of the mitogen activated protein 3 kinase, c-Raf ( Raf : ER ), CpG or LPS induction of IL-10 was only partially restored in nfkb1 ( -/- ) cells expressing Raf : ER, a finding consistent with NF-kappaB1 regulating IL-10 by a combination of ERK independent and -dependent mechanisms
Dubourdeau et al., J Immunol 2006 (MAP Kinase Signaling System) : Our investigations revealed that immunocompetent TLR2, TLR4 , and MyD88 knockout mice were not more susceptible to invasive aspergillosis as compared with wild-type mice and that the in vitro phosphorylation of the MAPKs ERK and p38 was not affected in TLR2, TLR4, or MyD88 knockout mice following stimulation with conidia
Kawakami et al., J Rheumatol 2007 (Sjogren's Syndrome) : TLR ligands induced phosphorylation of ERK , JNK, and p38 in HSG cells, but not Akt phosphorylation or activation of NF-kappaB p65
Lim et al., Exp Mol Med 2007 : Taken together, our data demonstrate that CpG ODN triggers MMP-9 expression via TLR-9 dependent ERK and p38 MAPK activation followed by NF-kappaB activation
Loniewski et al., Mol Immunol 2007 : In contrast to TLR4 signaling, TLR7 activation of ERK , JNK pathways and phosphorylation of p105 and I kappa B alpha are completely inhibited in TRAF6 knockdown cells ... These results suggest that while TRAF6 is absolutely essential for TLR7 activation of ERK, JNK and NF kappa B pathways, TLR4 induced ERK , JNK pathways and IKK mediated phosphorylation of I kappa B family members as well as cytokine expression are differentially sensitive to the cellular levels of TRAF6
West et al., Immunology 2008 (Vasculitis) : ISO-1 is a promising parent molecule which inhibits TLR induced ERK activation and inflammatory cytokine production in monocytes, whose role may be complicated by cell-type specificity
Park et al., Oncogene 2011 (Adenocarcinoma...) : Together, these findings suggest that the new cancer associated ligand, PAUF, may activate TLR mediated ERK signaling to produce the protumorigenic cytokines, but inhibits TLR mediated NF-?B signaling, thereby facilitating tumor growth and escape from innate immune surveillance