Gene interactions and pathways from curated databases and text-mining

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RELA — TLR10

Text-mined interactions from Literome

Horng et al., Nat Immunol 2001 : Although some cellular responses are completely abolished in MyD88-deficient mice, TLR4 , but not TLR9, can activate NF-kappa B and mitogen activated protein kinases and induce dendritic cell maturation in the absence of MyD88
An et al., Immunology 2002 : While inhibition of extracellular signal related kinase and NF-kappaB activation suppressed the up-regulation of the expression of TLR2, TLR4 and TLR9 mRNA, inhibition of p38 kinase prevented the up-regulation of TLR2 and TLR4 mRNA expression but enhanced the up-regulation of TLR9 expression
Takami et al., J Immunol 2002 : Moreover, various TLR ligands ( e.g., peptidoglycan, poly ( I:C ) dsRNA, LPS, and CpG motif of unmethylated DNA, which act as ligands for TLR2, 3, 4, and 9, respectively ) induced NF-kappa B activation and up-regulated TNF-alpha production in osteoclast precursor cells
Zhang et al., FEBS Lett 2002 : NF-kappaB activation by TLR2/1, TLR2/6 and the TLR4 monomer, but not TLR4/4, was completely inhibited by dominant negative MyD88, suggesting that TLR4 homodimers and monomers could activate NF-kappaB through different mechanisms
Jiang et al., J Biol Chem 2003 (MAP Kinase Signaling System) : However, we find that, in response to dsRNA, TLR3 can mediate the activation of both NFkappaB and mitogen activated protein ( MAP ) kinases in IL-1-unresponsive mutant cell lines, including IRAK-deficient I1A and I3A cells, which are defective in a component that is downstream of IL-1R but upstream of IRAK
Akira et al., J Infect Dis 2003 : After stimulation, TLR recruits IL-1R associated kinase via adaptor myeloid differentiation factor 88 ( MyD88 ) and induces activation of NF-kappaB and mitogen activated protein kinases
Janssens et al., FEBS Lett 2003 : MyD88 is an adapter protein that is involved in Toll-like receptor ( TLR ) - and interleukin-1 receptor (IL-1R) induced activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) ... MyD88 ( S ) is not able to activate NF-kappaB, and in contrast functions as a dominant negative inhibitor of TLR/IL-1R induced NF-kappaB activation
Akira et al., C R Biol 2004 : Upon stimulation, TLR recruits a cytoplasmic adaptor molecule MyD88, then IL-IR associated kinase ( IRAK ), and finally induces activation of NF-kappaB and MAP kinases
Pivarcsi et al., Acta Microbiol Immunol Hung 2004 : In response to challenge with microbes or microbial derived substances the activation and nuclear translocation of NF-kappaB , the production of nitric oxide ( NO ) and inflammatory cytokines occur in keratinocytes, in a TLR dependent manner
Seki et al., Hepatology 2005 : However, TLR2 , 4 and 9, which recognize gram negative and -positive bacterial products, are not essential for NF-kappaB activation and IL-6 production after PH, which excludes a possible contribution of TLR2/TLR4 or TLR9 to MyD88 mediated pathways
Bucki et al., Biochemistry 2005 : Additionally, TLR dependent NF-kappaB translocation in astrocytes appears to be blocked by gelsolin
Abujamra et al., Virology 2006 : Using Toll-like receptor ( TLR ) deficient HEK293 cells and PKR ( -/- ) mouse embryo fibroblasts, we further demonstrate that although dsRNA activated protein kinase R (PKR) is not necessary, TLR3 is required for the activation of NFkappaB by the LTR
Yamaguchi et al., FEBS Lett 2005 : Therefore, in the present study, we investigated whether globular adiponectin ( gAd ) would be able to inhibit TLR mediated nuclear factor-kappaB (NF-kappaB) signaling in mouse macrophages ( RAW264 ) ... gAd predominantly bound to the AdipoR1 receptor and suppressed TLR mediated NF-kappaB signaling ... gAd mediated inhibition of TLR mediated IkappaB phosphorylation and NF-kappaB activation was eliminated by the pretreatment of cycloheximide
Wang et al., Nat Immunol 2006 : Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating Toll-like receptor ( TLR ) -interleukin 1 receptor (IL-1R) signaling and subsequent activation of NF-kappaB and AP-1, transcriptional activators of innate immunity
Musette et al., Med Sci (Paris) 2006 (Infection...) : The TLR activation induce the NF-kappaB translocation to the nucleus and cytokine secretion
Minoda et al., Biochem Biophys Res Commun 2006 : Overexpression and knockdown by siRNA indicated that ZCCHC11 functions as a negative regulator of TLR mediated NF-kappaB activation
Qin et al., J Biol Chem 2006 : On the other hand, TLR8 mediated IkappaBalpha phosphorylation, NF-kappaB , and JNK activation are completely abolished in MEKK3 ( -/- ) MEFs, whereas IL-1 mediated signaling was only moderately reduced in these deficient MEFs as compared with wild-type cells
Takahashi et al., J Vet Med Sci 2006 : These observations suggest that immediate response of NODs to endotoxins could result from NF-kappaB activation via TLR signaling, whereas the second rise in NOD mRNAs might have resulted from TNF-alpha production possibly through NF-kappaB, TLR, and/or NOD signalings
Kataoka et al., Cell Microbiol 2006 : TLR2 ( N114A, N199A ), TLR2 ( N114A, N414A ) and, to a lesser extent, TLR2 ( N114A, N442A ), in which two N-linked glycans are speculated to be exposed to the concave surface of TLR2 solenoid, not only induce NF-kappaB activation but also are associated with wild-type TLR2 and TLR6
Jiang et al., Cell Res 2006 (Respiratory Distress Syndrome, Adult) : Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR dependent basal activation of NF-kappaB
Boyd et al., Cardiovasc Res 2006 (Myocarditis) : Using transfection of a nuclear factor kappa B (NF-kappaB)-Luciferase reporter plasmid, we found significantly increased NF-kappaB transcriptional activity in response to TLR2, TLR4 and TLR5 activation in cardiomyocytes
Ishihara et al., Curr Pharm Des 2006 (Gastrointestinal Diseases...) : In the intestine, TLR dependent activation of NF-kappaB plays a vital role in maintaining epithelial homeostasis as well as regulating infections and inflammation, while dysregulation of TLR signaling is associated with the pathogenesis of inflammatory bowel diseases ( IBD )
Asakura et al., Am J Hematol 2007 : Here we show that ectopic overexpression of catalytically inactive dominant negative PKR expression system suppressed NF- kappa B activation mediated by TLR3, TLR9 , TNF receptor 1 and 2 (TNF-R 1/2), but not by TLR4
Shamshiev et al., J Exp Med 2007 (Dyslipidemias...) : We found that oxidized low-density lipoprotein ( oxLDL ) was the key active component responsible for this effect, as it could directly uncouple TLR mediated signaling on CD8alpha ( - ) myeloid DCs and inhibit NF-kappaB nuclear translocation
Carmody et al., Cell Mol Immunol 2007 (Infection) : Many of the key molecular events required for TLR induced NF-kappaB activation have been elucidated
Gringhuis et al., Immunity 2007 : We demonstrated that pathogens trigger DC-SIGN on human DCs to activate the serine and threonine kinase Raf-1, which subsequently leads to acetylation of the NF-kappaB subunit p65, but only after TLR induced activation of NF-kappaB
Karrasch et al., J Immunol 2007 (Colitis...) : We conclude that bacteria induced experimental colitis involves the activation of TLR induced NF-kappaB signaling derived mostly from mucosal immune cells ... Blocking TLR induced NF-kappaB activity may represent an attractive strategy to treat immune mediated intestinal inflammation
Weersma et al., Scand J Gastroenterol 2007 (Colitis, Ulcerative...) : The interleukin receptor associated kinase-M ( IRAK-M ) is a NF-kappaB mediated , negative regulator of Toll-like receptor ( TLR ) signaling
Lundberg et al., Blood 2007 (Inflammation) : Furthermore, TLR3 stimulation did not activate NFkappaB , MAPKs, or IRF-3 in DCs and MOs, but was able to do so in ECs and RA-SF
Yamamoto et al., J Exp Med 2007 : Microarray analysis showed that Trib1-deficient macrophages exhibited a dysregulated expression pattern of lipopolysaccharide-inducible genes, whereas TLR mediated activation of MAP kinases and NF-kappaB was normal
Kubo-Murai et al., J Biochem 2008 : IRAK-4 dependent degradation of IRAK-1 is a negative feedback signal for TLR mediated NF-kappaB activation ... These results suggested that the expression of IRAK-4 alone is sufficient to cause the degradation of IRAK-1 ; the autophosphorylation of IRAK-1 is not necessary to terminate the TLR induced activation of NF-kappaB
Shi et al., Nat Immunol 2008 : Our results collectively indicate that TRIM30alpha negatively regulates TLR mediated NF-kappaB activation by targeting degradation of TAB2 and TAB3 by a ` feedback ' mechanism
Xu et al., Mol Immunol 2008 : PTP1B inhibits TLR ligands induced activation of MAPKs, NF-kappaB , and IRF3, furthermore, co-transfection of PTP1B inhibits both MyD88- and TRIF induced transcription of TNF-alpha and IFN-beta reporter genes in a dose dependent manner
van Keulen et al., Atherosclerosis 2009 (Carotid Artery Diseases...) : Tlr activation results in nuclear translocation of the transcription factor Nuclear Factor-kappa B (NF-kappaB) that controls the transcription of many inflammatory genes
Zheng et al., Infect Immun 2008 : Taken together, our results demonstrate that Campylobacter induced IL-8 secretion requires functional flagella and CDT and depends on the activation of NF-kappaB through TLR signaling and CDT in human intestinal epithelial cells
Sugiyama et al., Eur J Pharmacol 2008 (Shock, Septic) : STM28 showed no inhibitory effects against NF-kappaB activation induced by TLR1/2, TLR3 and TLR9 ligands in a mouse macrophage cell line, RAW 264
Fraczek et al., J Biol Chem 2008 : Two parallel interleukin-1 (IL-1) mediated signaling pathways have been uncovered for IL-1R-TLR mediated NFkappaB activation : TAK1 dependent and MEKK3 dependent pathways, respectively ... Deletion analysis of IRAK4 indicates the essential structural role of the IRAK4 death domain in receptor proximal signaling for mediating IL-1R-TLR induced NFkappaB activation
Shin et al., PLoS Pathog 2008 : This enhanced response involved NF-kappaB activation by TLR signaling as well as Nod1 and Nod2 detection of type IV secretion
Shah et al., Neurosci Lett 2009 : At the molecular level, beta-glucan suppressed TLR mediated NF-kappaB activation, which may be responsible for the diminished capacity of microglia to produce cytokines in response to TLR stimulation
Maitra et al., Journal of inflammation (London, England) 2009 : Activation of the transcription factor NFkappaB through Toll-like receptors ( TLR ) following bacterial infection is principally involved in regulating lung inflammation in CF. NFkappaB regulates the transcription of several genes that are involved in inflammation, anti-apoptosis and anti-microbial activity, and hyper-activation of this transcription factor leads to a potent inflammatory response
Yoshimi et al., J Immunol 2009 : Reporter analyses demonstrated that TLR mediated NF-kappaB activation was higher in Trim21 ( -/- ) cells than in wild-type cells, most likely accounting for their enhanced cytokine expression
Logunov et al., Mol Gen Mikrobiol Virusol 2009 : Various strains of mycoplasmas cause activation of transcriptional factor NF-kB as a result of interaction with different combinations of Toll-like receptors ( TLR )
Gao et al., Cell Mol Life Sci 2009 : Transforming growth factor-beta activated kinase 1 ( TAK1 ) is a serine/threonine protein kinase that is critically involved in the activation of NF-kappaB by tumor necrosis factor ( TNFalpha ), interleukin-1beta (IL-1beta) and TLR ligands
Brownlie et al., Mol Immunol 2009 : In this study, chicken TLRs 7, 15 and 21 were expressed in mammalian HEK-293T cells ; expression of TLR21 but not TLR7 or 15 resulted in marked NF-kappaB activation upon stimulation with exogenous ODN ... TLR21 mediated NF-kappaB activation in HEK-293T cells was inhibited by bafilomycin A suggesting that endosomal maturation is required for TLR21 activation and observations by confocal microscopy and digestion with endoglycosidase H suggest TLR21 localizes to the endoplasmic reticulum ( ER ) of resting cells
Verstak et al., J Biol Chem 2009 (Bacterial Infections...) : We have previously reported an interaction between Mal and tumor necrosis factor receptor associated factor 6 ( TRAF6 ) via a TRAF6 binding motif, the disruption of which inhibited TLR mediated NF-kappaB-luciferase reporter activity
Huang et al., J Clin Microbiol 2009 : The assay readout is the induction of NF-kappaB and/or cytokines in response to TLR activation
He et al., Clinical and vaccine immunology : CVI 2009 (Mycoplasma Infections) : The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6 , and CD14
Boyd et al., J Immunol 2009 : Specifically, we demonstrate the Siglec-E expression inhibits TLR induced NF-kappaB and more importantly, the induction of the antiviral cytokines IFN-beta and RANTES
Premkumar et al., BMC chemical biology 2010 : Also, the suppressive effect of triptolide on TLR induced NFkappaB activation was observed when either MyD88 or TRIF was knocked out, confirming that both MyD88 and TRIF mediated NFkappaB activation may be inhibited by triptolide
Chaurasia et al., Mol Cell Biol 2010 (Sepsis) : These experiments reveal a novel PDK-1 dependent negative feedback inhibition of TLR induced NF-kappaB activation in macrophages in vivo
Cantu et al., Am J Transplant 2013 (Primary Graft Dysfunction) : Three hundred sixty-two gene sets were upregulated, with eight meeting significance ( familywise-error rate, FWER p-value < 0.05 ), including the NOD-like receptor inflammasome ( NLR ; p < 0.001 ), toll-like receptors ( TLR ; p < 0.001 ), IL-1 receptor ( p = 0.001 ), myeloid differentiation primary response gene 88 ( p = 0.001 ), NFkB activation by nontypeable Haemophilus influenzae ( p = 0.001 ), TLR4 ( p = 0.008 ) and TLR 9 ( p = 0.018 )