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IRF6 — MYD88

Text-mined interactions from Literome

Kaisho et al., J Immunol 2001 : All of them were completely abolished in MyD88-deficient mice, indicating the essential role of MyD88 in LPS signaling
Byrd-Leifer et al., Eur J Immunol 2001 : To determine whether TLR4 and its interacting adaptor molecule MyD88 are necessary for Taxol 's LPS mimetic actions, we examined Taxol responses of primary macrophages from genetically defective mice lacking either TLR4 ( C57BL/10ScNCr ) or MyD88 ( MyD88 knockout )
Bannerman et al., J Biol Chem 2002 : Using a variety of dominant negative constructs, we have identified a role for MyD88 and interleukin-1 receptor associated kinase-1 ( IRAK-1 ) in mediating LPS pro-apoptotic signaling in human endothelial cells
Kaisho et al., Int Immunol 2002 : In this study, we have further characterized function of LPS stimulated , MyD88 ( -/- ) DC
Medvedev et al., J Immunol 2002 : Dysregulation of LPS induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor associated kinase 1 activation in endotoxin-tolerant cells ... LPS induced the association of MyD88 with TLR4 and increased IRAK-1 activity in medium pretreated cells
Oshikawa et al., Biochem Biophys Res Commun 2003 (Lung Diseases) : The results demonstrated three patterns of gene expression : the TLR2 and myeloid differentiation factor 88 ( MyD88 ) gene expressions were induced in AM in response to lipopolysaccharide (LPS) , interleukin (IL)-1beta, or tumor necrosis factor-alpha or in the lung tissue of an LPS induced acute lung injury model ; the gene expressions of TLR1, -3, -6, CD14, and MD2 were unchanged ; and the TLR4 and TLR5 gene expressions were downregulated in AM following inflammatory stimuli
Tamai et al., J Endotoxin Res 2003 : LPS and IFN-gamma alone each augmented MD-2 and MyD88 mRNA expression in THP-1 cells, and co-stimulation with LPS and IFN-gamma markedly enhanced MD-2 and MyD88 mRNA expression in the cells compared to those with either LPS or IFN-gamma alone
Hirotani et al., Biochem Biophys Res Commun 2005 : Surprisingly, 80 LPS-inducible genes were redundantly regulated by either MyD88 or TRIF
Li et al., J Leukoc Biol 2006 : Furthermore, decreased MyD88-IRAK immunocomplex formation, as demonstrated by immunoprecipitation, was observed in BLP-tolerant cells following a second BLP or LPS stimulation
Esen et al., J Immunol 2006 : Microglial activation was only partially inhibited in LPS stimulated MyD88 KO cells, suggesting the involvement of MyD88 independent pathways
Sacre et al., J Immunol 2007 : Previously, we showed that MyD88 or Mal dominant negative constructs did not inhibit LPS induction of cytokines in primary human M-CSF derived macrophages
Zanin-Zhorov et al., J Immunol 2007 : This response to LPS was confirmed in mouse T cells ; functional TLR4 and MyD88 were required , but T cells from TLR2 knockout mice could respond to LPS
McAleer et al., J Immunol 2007 : LPS induced long-term survival of superantigen stimulated CD4 and CD8 T cells in a MyD88 dependent manner
Zhao et al., Am J Chin Med 2008 : The results indicate that LPS increased the expression of TLR4, MyD88 , TRAF-6, TRAM and TRIF, but had no influence on TLR3, while poly ( I:C ) up-regulated the expression of TLR3, MyD88, TRAM and TRIF
Lee et al., Mol Cells 2008 : Stimulation of TLR4 by LPS activates both myeloid differential factor 88 (MyD88)- and TIR domain containing adapter inducing IFNbeta ( TRIF ) -dependent signaling pathways leading to activation of NF-kappaB and IFN-regulatory factor 3 (IRF3)
Dagvadorj et al., Innate Immun 2008 : Although the level of MyD88 protein increased in response to LPS , IL-10 prevented the LPS induced MyD88 augmentation
Kanuri et al., J Nutr 2009 (Fatty Liver) : In vitro prechallenge with cinnamon extract suppressed lipopolysaccharide (LPS) induced MyD88 , iNOS, and TNFalpha expression as well as NO formation almost completely
Uh et al., Reproductive biology and endocrinology : RB&E 2009 : Here we investigated the role of MyD88 , TRIF and IRAK2 on cAMP induced CRH promoter activation in JEG3 cells in the absence of LPS/TLR4 stimulation
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
Dean et al., Brain Behav Immun 2010 : These data suggest that MyD88 dependent activation of microglia by LPS causes release of factors directly toxic to neurons
Anas et al., PloS one 2010 (Acute Disease...) : Recently, in vitro studies revealed that CD14 is required for activation of the myeloid differentiation factor (MyD)88 dependent Toll-like receptor (TLR)4 signaling pathway by smooth ( S ) -LPS , but not by rough ( R ) -LPS
Buchholz et al., Am J Physiol Gastrointest Liver Physiol 2010 (Ileus) : LPS induced MyD88 and TRIF mRNA upregulation was quantified within the intestinal muscularis of TLR4-competent and TLR4-mutant mice, and MyD88 mRNA levels were additionally measured in TLR4 bone marrow chimeras ... LPS induction of the primary downstream signaling element MyD88 was TLR4 dependent and was derived in equal amounts from both the hematopoietic and the nonhematopoietic cells
Van Linthout et al., J Mol Med (Berl) 2011 (Inflammation) : In vitro, supplementation of HDL or apo A-I to human microvascular endothelial cells-1 24 h before LPS administration reduced TLR4 expression, as assessed by fluorescent activated cell sorting, and decreased the LPS induced MyD88 mRNA expression and NF-?B activity, independently of LPS binding
Kezic et al., J Leukoc Biol 2011 (Uveitis) : TLR4 activation by LPS ( endotoxin ) is mediated by the MyD88 and TRIF intracellular signaling pathways
Kissner et al., J Biol Chem 2011 (Inflammation...) : Furthermore, LPS induced MyD88 signaling was likewise inhibited in a cell based reporter assay
Ren et al., Immunol Lett 2011 (Pneumonia) : Myeloid differentiation protein 2 silencing decreases LPS induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages
Butt et al., J Biol Chem 2012 (Inflammation) : Interestingly, although the 14-3-3 proteins inhibit poly ( I:C ) -mediated RANTES production, 14-3-3 proteins augment Pam ( 3 ) CSK ( 4 ), LPS , R848, and CpG mediated production of RANTES ( regulated on activation normal T cell expressed and secreted ) in a Mal ( MyD88 adaptor-like ) /MyD88 dependent manner
Lee et al., Cell communication and signaling : CCS 2012 : We observed that LPS induced TLR4, MyD88 , c-Src, and p47phox complex formation determined by co-immunoprecipitation and Western blot
Srivastava et al., Journal of cell communication and signaling 2013 : Quantitative RT-PCR analysis show that LPS differentially up-regulated the expression of genes for TLRs ( 1? > ?4?=?2? > ?3? > ?6? > ?5 ), the adapter molecule, MyD88 , and transcription factor NF-?B within one hour
Zhu et al., Int Immunopharmacol 2013 (Disease Models, Animal...) : BAY 11-7082 could not simultaneously inhibit LPS induction of TLR4, MyD88 and ß-glucan activation of Dectin1/Syk in rat mammary epithelial cells ... These findings demonstrated that ß-glucan activation of Dectin1/Syk attenuated LPS induction of TLR4/MyD88/NF-?B and inhibited the LPS induced inflammation factors in mammary epithelial cells, thereby providing a possibly protective effect of ß-glucan in the prevention of LPS induced dysfunction in mammary epithelial cells
Zhang et al., Zhongguo Ying Yong Sheng Li Xue Za Zhi 2013 : LPS could increase MyD88 and TRAF6 mRNA, upregulate protein level of MyD88 and TRAF6 and increase the level of TNF-alpha, IL-1beta and NO in cell culture supernatant