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IL6 — MYD88

Text-mined interactions from Literome

Schilling et al., J Immunol 2002 : TLR4 dependent induction of IL-6 expression did require Toll-IL-1R domain containing adapter protein ( TIRAP ) /MyD88 adapter-like (Mal) , but unlike iNOS and IP-10, it did not require the expression of IFN-beta
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
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)
Senn et al., J Biol Chem 2006 (Insulin Resistance) : RNA interference mediated inhibition of TLR2 and MyD88 expression in C2C12 muscle cells resulted in a near complete inhibition of palmitate induced insulin resistance and IL-6 production
Sacre et al., Am J Pathol 2007 (Arthritis, Rheumatoid...) : In addition, overexpression of dominant negative forms of MyD88 and Mal/TIRAP significantly down-regulated the spontaneous production of cytokines tumor necrosis factor-alpha, IL-6 , and vascular endothelial growth factor, and enzymes MMP-1, MMP-2, MMP-3, and MMP-13 in RA synovial membrane cell cultures
Naugler et al., Science 2007 (Liver Neoplasms, Experimental...) : Gender disparity in liver cancer due to sex differences in MyD88 dependent IL-6 production
Rad et al., Gastroenterology 2007 (Gastritis...) : The adaptor protein Myd88 mediates Toll-like receptor ( TLR ), interleukin (IL)-1 , and IL-18 signaling
Mizobe et al., Exp Hematol 2007 (Cell Transformation, Viral) : 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
Salazar-Gonzalez et al., J Immunol 2007 (Salmonella Infections) : IL-6 production, increased expression of activation markers, and dendritic cell redistribution in the spleen were dependent on MyD88 expression by bone marrow derived cells
Prieto et al., J Hepatol 2008 : Gender disparity in liver cancer due to sex differences in MyD88 dependent IL-6 production
Marta et al., Eur J Immunol 2008 (Encephalomyelitis, Autoimmune, Experimental) : Our data suggest that MyD88 mediates the induction of mDC IL-6 and IL-23 responses after MOG immunization, which in turn drives IL-17 producing encephalitogenic Th17 cell activation
Lee et al., J Invest Dermatol 2009 : Overexpression of MyD88wt and MyD88DeltaC, but not of MyD88DeltaN, increased the basal expressions of IL-6 and matrix metalloproteinase-1 (MMP-1) in human epidermal keratinocytes ... Moreover, overexpression of MyD88DeltaN prevented UV-induced expressions of IL-6 and MMP-1 by inhibiting UV-induced activation of NF-kappaB and activating protein-1
Lichtnekert et al., American journal of physiology. Renal physiology 2009 (Glomerulonephritis...) : Exposure to necrotic cells activated cultured primary mesangial cells to produce Il-6 in a Tlr2/Myd88 dependent manner ... Apoptotic cell induced Il-6 release was Myd88 dependent , and only purified apoptotic cell RNA induced Trif signaling in mesangial cells
Leichtle et al., BMC immunology 2009 (Otitis Media) : Activated TLRs signal via two alternative intracellular signaling molecules with differing effects ; MyD88 ( Myeloid differentiation primary response gene 88 ) inducing primarily interleukin expression and TRIF ( Tir-domain containing adaptor inducing interferon beta ) mediating type I interferon ( IFN ) expression
Griffith et al., J Immunol 2009 (Inflammation...) : MCP-1 and KC are produced independently of MyD88, TLR2/4 and TLR9, and components of the inflammasome ; however, neutrophil recruitment, the localized production of IL-1beta, and the increase in circulating IL-6 require MyD88 signaling, the IL-1R pathway, and the inflammasome components ICE ( IL-1beta converting enzyme ), ASC ( apoptosis associated, speck-like protein containing CARD ), and NALP3
Hoshino et al., J Leukoc Biol 2010 (MAP Kinase Signaling System) : HIV-1 Vpr induces TLR4/MyD88 mediated IL-6 production and reactivates viral production from latency ... The induction of IL-6 by rVpr was dependent on signaling through TLR4 and its adaptor molecule, MyD88
Kissner et al., Innate Immun 2011 (Disease Models, Animal...) : Our results indicated that elevated tumor necrosis factor-a, interferon-?, interleukin (IL)-1a/ß and IL-6 production from mouse spleen cells treated with SEB alone or in combination with lipopolysaccharide (LPS) was regulated by MyD88
Ather et al., J Immunol 2011 (Disease Models, Animal...) : Furthermore, SAA drives production of IL-1a, IL-1ß, IL-6 , IL-23, and PGE ( 2 ), causes dendritic cell ( DC ) maturation, and requires TLR2, MyD88 , and the NLRP3 inflammasome for secretion of IL-1ß by DCs and macrophages
Klaas et al., J Immunol 2012 : This was accompanied by a strong reduction in MyD88 dependent secretion of TNF-a, IL-6 , IL-12, and IL-10
Sjölinder et al., Infect Immun 2012 : Interleukin-6 (IL-6) secretion was dependent on activation of TLR4 and required the TLR signaling adaptor protein MyD88
Cheng et al., International journal of biological sciences 2013 : Silencing MyD88 , but not TRIF, inhibited AGE-LDL induced IL-6 and IL-8 production
Liu et al., J Neurosci 2013 : In cultured neurons, TLR7 activation induced IL-6 and TNF-a expression through Myd88