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MYD88 — RELA

Text-mined interactions from Literome

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
Burns et al., J Exp Med 2003 : In the presence of MyD88s , IRAK-1 is not phosphorylated and neither activates NF-kappaB nor is ubiquitinated
Yeo et al., J Biol Chem 2003 : Conclusively, these results demonstrate that endosomal DNA processing and TLR9/MyD88 dependent activation of NF-kappaB and p38 are required for transcriptional regulation of Cox-2 expression induced by CpG DNA, and suggest that interleukin-1 receptor associated kinase and/or TRAF6 may be a diverging point for NF-kappaB activation in response to CpG DNA in RAW264.7 cells
Lee et al., J Biol Chem 2003 : Saturated fatty acid ( lauric acid ) -induced NFkappaB activation was inhibited by a dominant negative mutant of TLR4, MyD88 , IRAK-1, TRAF6, or IkappaBalpha in macrophages ( RAW264.7 ) and 293T cells transfected with TLR4 and MD2 ... AKT ( DN ) blocked MyD88 induced NFkappaB activation, suggesting that AKT is a MyD88 dependent downstream signaling component of TLR4 ... DHA also suppressed NFkappaB activation induced by TLR4 ( CA ), but not MyD88 ( CA ) or AKT ( CA ), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT
Andreakos et al., Blood 2004 : We found that MyD88 and Mal/TIRAP are essential for LPS induced I kappa B alpha phosphorylation, NF-kappa B activation, and interleukin 6 (IL-6) or IL-8 production in fibroblasts and endothelial cells in a pathway that also requires IKK2 ... In contrast, in macrophages neither MyD88 , Mal/TIRAP, nor I kappa B kinase 2 (IKK2) are required for NF-kappa B activation or tumor necrosis factor alpha (TNF alpha), IL-6, or IL-8 production, although Mal/TIRAP is still involved in the production of interferon beta (IFN beta)
Xiong et al., Virology 2004 : Using a nuclear factor-kappaB (NF-kappaB) dependent reporter assay, it was shown that activation of NF-kappaB was moderately increased in the presence of expression of MyD88 , and further significantly increased by co-expression of HBV
Platz et al., J Immunol 2004 : Up-regulation of NF-kappaB in epithelial cells in response to the CpG motif containing DNA was inhibited by overexpression of a dominant negative form of MyD88
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
Flemming et al., Cell Immunol 2004 : Disruption of membrane cholesterol stimulates MyD88 dependent NF-kappaB activation in immature B cells
Chen et al., Biochem Biophys Res Commun 2004 : Moreover, P6 induces MUC5AC transcription via TLR2-MyD88-IRAK1-TRAF6-TAK1 dependent p38 MAPK-AP1 and IKKbeta-IkappaBalpha-NF-kappaB signaling pathways
Sacre et al., J Endotoxin Res 2004 : In cell lines and murine models, parts of the signaling pathways involved have been elucidated with MyD88 , Mal/TIRAP and IKK2 playing an important role in the induction of NF-kappaB ... We show that in primary human macrophages MyD88 , Mal/TIRAP and IKK2 independent alternative pathways activate NF-kappaB and induce the expression of inflammatory cytokines, whereas in non-myeloid synovial fibroblasts MyD88 and/or Mal/TIRAP are essential adaptors for LPS signaling
Li et al., J Mol Med (Berl) 2005 : LPS induced, TLR4 mediated signaling employs multiple TIR-domain containing adaptors, MyD88/TIRAP to mediate NFkappaB activation, TRIF/TRAM for IRF3 activation
Li et al., Zhonghua Yi Xue Za Zhi 2005 (Cardiomegaly) : MyD88 dependent NFkappaB signaling is a novel pathway for inducing the development of cardiac hypertrophy in vivo and blocking MyD88 mediated signaling pathway attenuates the development of cardiac hypertrophy
Youn et al., J Immunol 2005 : Further, resveratrol inhibited NF-kappaB activation induced by TRIF, but not by MyD88
Carroll et al., J Immunol 2005 (Inflammation) : In contrast, only MyD88delta was found to inhibit IL-1 induced NF-kappaB reporter activity
Ness et al., J Immunol 2006 (Bacterial Infections...) : MyD88 dependent NF-kappaB signaling was significantly down-regulated in CCR4 ( -/- ) macrophages, whereas p38 MAPK and JNK activation were conversely increased
Koide et al., J Endotoxin Res 2007 : LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-gamma stimulated END-D cells, although it did not affect the activation of either MyD88 dependent nuclear factor (NF)-kappaB or MyD88 independent IRF-3
Youn et al., Biochem Pharmacol 2008 : Cinnamaldehyde did not inhibit the activation of NFkappaB or IRF3 induced by MyD88 dependent ( MyD88, IKKbeta ) or TRIF dependent ( TRIF, TBK1 ) downstream signaling components
Mizobe et al., Exp Hematol 2007 (Cell Transformation, Viral) : In this study, we investigated whether MyD88 , an adaptor protein of Toll-like receptor ( TLR ) signaling, contributes to constitutive NF-kappaB activation in HTLV-I transformed T cells ... Constitutive activation of NF-kappaB and NF-IL-6 and cytokine gene promoters, such as IL-1alpha, interferon-gamma, and tumor necrosis factor-alpha in MT2 cells was inhibited by MyD88dn expression
Lin et al., Biochim Biophys Acta 2007 : The MyD88 activated nuclear factor-kappaB (NF-kappaB) signaling pathway and the intracellular upregulation of NF-kappaB signaling can induce an antiviral effect
Youn et al., Int Immunopharmacol 2008 : Selenium inhibited NF-kappaB activation induced by poly [ I:C ] ( TLR3 agonist ), LPS ( TLR4 agonist ) or overexpression of MyD88 or IKK-beta which is the key kinase of MyD88 dependent signaling pathway
Torgler et al., J Immunol 2008 (Malaria) : Sporozoite mediated hepatocyte wounding limits Plasmodium parasite development via MyD88 mediated NF-kappa B activation and inducible NO synthase expression
Ahn et al., Exp Dermatol 2008 : LPS upregulated the expression of TLR4 and MyD88 and induced NF-kappaB nuclear translocation B nuclear translocation in melanocytes
Lee et al., Mol Cells 2008 : Acrolein inhibited NF-kappaB and IRF3 activation by LPS, but it did not inhibit NF-kappaB or IRF3 activation by MyD88 , inhibitor kappaB kinase (IKK)beta, TRIF, or TNF-receptor associated factor family member associated NF-kappaB activator ( TANK) binding kinase 1 (TBK1 )
Hatao et al., FEMS Immunol Med Microbiol 2008 : Expression of either a deletion mutant of MyD88 lacking its death domain or MyD88s, neither of which induced NF-kappaB activation , did not lead to IRAK-4 downregulation
Rallabhandi et al., J Biol Chem 2008 (Inflammation) : In the absence of TLR4, PAR2 induced NF-kappaB activity was inhibited by dominant negative ( DN ) -TRIF or DN-TRAM constructs, but not by DN-MyD88 , findings confirmed using cell-permeable, adapter-specific BB loop blocking peptides
Bhattacharyya et al., Inflamm Bowel Dis 2009 : DSS induced increases in phospho-IkappaBalpha, nuclear NFkappaB ( p65 ), and IL-8 secretion in human colonic epithelial cells in tissue culture are attributable to a reactive oxygen species ( ROS ) -induced pathway of inflammation, and do not require TLR4, MyD88 , or Bcl10, which are associated with the innate immune pathway of NFkappaB-IL-8 activation
Filipovich et al., Am J Obstet Gynecol 2009 (Escherichia coli Infections...) : Intrauterine fetal survival, maintenance of circulating progesterone levels, and nuclear translocation of NFkappaB were also dependent upon MyD88 but not TRIF
Verstak et al., J Biol Chem 2009 (Bacterial Infections...) : MyD88 adapter-like (Mal)/TIRAP interaction with TRAF6 is critical for TLR2- and TLR4 mediated NF-kappaB proinflammatory responses
Loiarro et al., J Biol Chem 2009 : Moreover, overexpression of a green fluorescent protein ( GFP ) -tagged mini-MyD88 protein ( GFP-MyD88- ( 27-72 ) ), comprising the Glu ( 52 ) and Tyr ( 58 ) residues, interfered with recruitment of both IRAK1 and IRAK4 by MyD88 and suppressed NF-kappaB activation by the interleukin-1 receptor but not by the MyD88 independent TLR3
Amith et al., Cell Signal 2010 : Here, we show that endotoxin lipopolysaccharide (LPS) induced MyD88/TLR4 complex formation and subsequent NFkappaB activation is dependent on the removal of alpha-2,3-sialyl residue linked to beta-galactoside of TLR4 by the Neu1 activity associated with LPS stimulated live primary macrophage cells, macrophage and dendritic cell lines but not with primary Neu1-deficient macrophage cells
Langlet et al., Eur J Immunol 2010 : Dominant negative PKC-alpha inhibited NF-kappaB reporter activity mediated by overexpression of MyD88 but not TRIF
Zheng et al., J Immunol 2010 : In addition to promoting both MyD88- and TLR/IL-1 receptor domain containing adaptor protein inducing IFN-beta dependent MAPKs and NF-kappaB activation, Gab1 enhances PI3K/Akt activation by directly binding p85 in TLR signaling and VSV infection
Li et al., Am J Nephrol 2010 (Diabetes Mellitus, Experimental...) : The expression of TLR2 mRNA and protein level was significantly upregulated in the kidneys of diabetic rats ( p < 0.01 ), which was associated with increased renal expression of MyD88 and MCP-1, activation of NF-kappaB and infiltration of macrophages
Liu et al., J Immunol 2010 : Zebrafish Myd88 alone strongly induced the activation of NF-kappaB and IFN-beta both in HEK293T and carp leukocyte cells
Kissner et al., PloS one 2011 (Inflammation) : Here we report that human monocytes treated with SEA, SEB, or anti-MHC class II monoclonal antibodies up regulated MyD88 expression, induced activation of NF-kB , and increased expression of IL-1R1 accessory protein, TNF-a and IL-1ß
Burns et al., J Biol Chem 1998 : Overexpression of MyD88 induces activation of the c-Jun N-terminal kinase (JNK) and the transcription factor NF-kappaB through its DD ... MyD88 induced NF-kappaB activation is inhibited by the dominant negative versions of TRAF6 and IRAK, which also inhibit IL-1 induced NF-kappaB activation ... Overexpression of MyD88-lpr or MyD88-Toll ( expressing only the Toll domain ) acted to inhibit IL-1 induced NF-kappaB and JNK activation in a 293 cell line overexpressing the IL-1RI