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These results show that isofraxidin binds to and inhibits MD-2, thus preventing TLR4/MD-2 complex formation without altering TLR2 signalling. We demonstrated that isofraxidin promoted cell proliferation and inhibited the lipopolysaccharide induced inflammatory response through suppressing the activation of the TLR4/MD-2 axis and NF-kappaB signalling in human osteoarthritis chondrocytes.
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An increase of MD-2 expression levels was associated with an absolute mortality risk increase in dilated cardiomyopathy patients.
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sTLR4/MD-2 complex inhibits colorectal cancer migration and invasiveness in vitro and in vivo by lncRNA H19 down-regulation.
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MD-2 siRNA or plasmid further confirmed the efficacy of Iturin A by suppressing MD-2/TLR4 signaling pathway. The in silico docking study showed that the Iturin A interacted well with the MD-2 in MD-2/TLR4 receptor complex. Conclusively, inhibition of MD-2/TLR4 complex with Iturin A offered strategic advancement in cancer therapy.
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data confirm that engineered human cells expressing TLR4, MD2 and CD14 can respond to CMP with NF-kappaB activation and the response can be influenced by variations in CMP-mannosylation
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The observations suggest that MD-2 helps to regulate lipopolysaccharide-induced NLRP3 inflammasome activation and the inflammatory response in NR8383 cells, and likely does so by affecting MyD88/NF-kappaB signaling.
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MD2 plays an important role in induction of allergic sensitization to cat dander and common pollens relevant to human allergic diseases.
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we report that exogenous CnB is taken up by cells in a time- and concentration-dependent manner via clathrin-dependent receptor-mediated internalization. Our findings further confirm that uptake is mediated by the TLR4/MD2 complex together with the co-receptor CD14
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In this study, a novel naturally occurring spliceosome of human MD2, termed as MD2-T3, has been identified.
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Results show that cigarette smoke may alter innate immune responses reducing the expression of the MD2, a molecule with an important role in TLR4 signaling.
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Predominantly hydrophobic interactions between MD-2 and TLR4 contribute to the stabilization of the TLR4/MD-2/metal ion complex in a conformation that enables activation.
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The intensity of the intra-amniotic inflammatory response to bacteria or perhaps to other TLR4 ligands may be facilitated through synthesis and release of sMD2 by the amniochorion.
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Three genes (LY96, IL8 DPR) were significantly downregulated over time. This finding was confirmed in a validation cohort of stroke patients (n=8).
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The study revealed the impact of specific residues and regions of MD-2 on the binding of lipolysaccharides and TLR4.
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Gene polymorphisms of MD2 and GM2A were associated with the occurrence or severity of neonatal necrotizing enterocolitis.
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In patients undergoing CABG surgery, we found genetic polymorphisms in LY96 associated with decreased risk of postoperative AF.
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Aminoarabinose residues in lipid A contribute to Burkholderia lipid A binding to the TLR4.Myeloid Differentiation Factor 2 complex.
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TLR4 along with its accessory protein MD-2 builds a heterodimeric complex that specifically recognizes lipopolysaccharides, which are present on the cell wall of gram-negative bacteria, activating the immune response. (Review)
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genetic polymorphism is associated with asthma exacerbations in children
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In monocytes of sepsis, MD-2 expression was found to be regulated by STAT1.
