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anti-Human LY96 Antibodies:
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Human Polyclonal LY96 Primary Antibody for IHC (p), IHC - ABIN252602
Kunda, Cavicchia, Acosta: Lipopolysaccharides and trophic factors regulate the LPS receptor complex in nodose and trigeminal neurons. in Neuroscience 2014
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Human Monoclonal LY96 Primary Antibody for FACS, InhA - ABIN2192085
Pugin, Stern-Voeffray, Daubeuf, Matthay, Elson, Dunn-Siegrist: Soluble MD-2 activity in plasma from patients with severe sepsis and septic shock. in Blood 2004
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Human Monoclonal LY96 Primary Antibody for FACS - ABIN2192086
Daubeuf, Mathison, Spiller, Hugues, Herren, Ferlin, Kosco-Vilbois, Wagner, Kirschning, Ulevitch, Elson: TLR4/MD-2 monoclonal antibody therapy affords protection in experimental models of septic shock. in Journal of immunology (Baltimore, Md. : 1950) 2007
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Human Monoclonal LY96 Primary Antibody for FACS - ABIN2192087
Elson, Dunn-Siegrist, Daubeuf, Pugin: Contribution of Toll-like receptors to the innate immune response to Gram-negative and Gram-positive bacteria. in Blood 2007
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sTLR4/MD-2 complex inhibits colorectal cancer migration and invasiveness in vitro and in vivo by lncRNA H19 (show NCKAP1 Antibodies) down-regulation.
MD-2 siRNA or plasmid further confirmed the efficacy of Iturin A by suppressing MD-2/TLR4 (show TLR4 Antibodies) signaling pathway. The in silico docking study showed that the Iturin A interacted well with the MD-2 in MD-2/TLR4 (show TLR4 Antibodies) receptor complex. Conclusively, inhibition of MD-2/TLR4 (show TLR4 Antibodies) complex with Iturin A offered strategic advancement in cancer therapy.
data confirm that engineered human cells expressing TLR4 (show TLR4 Antibodies), MD2 and CD14 (show NDUFA2 Antibodies) can respond to CMP (show MATN1 Antibodies) with NF-kappaB (show NFKB1 Antibodies) activation and the response can be influenced by variations in CMP (show MATN1 Antibodies)-mannosylation
The observations suggest that MD-2 helps to regulate lipopolysaccharide-induced NLRP3 (show NLRP3 Antibodies) inflammasome activation and the inflammatory response in NR8383 cells, and likely does so by affecting MyD88 (show MYD88 Antibodies)/NF-kappaB (show NFKB1 Antibodies) signaling.
MD2 plays an important role in induction of allergic sensitization to cat dander and common pollens relevant to human allergic diseases.
we report that exogenous CnB (show PPP3R1 Antibodies) 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 (show TLR4 Antibodies)/MD2 complex together with the co-receptor CD14 (show NDUFA2 Antibodies)
In this study, a novel naturally occurring spliceosome of human MD2, termed as MD2-T3, has been identified.
Results show that cigarette smoke may alter innate immune responses reducing the expression of the MD2, a molecule with an important role in TLR4 (show TLR4 Antibodies) signaling.
Predominantly hydrophobic interactions between MD-2 and TLR4 (show TLR4 Antibodies) contribute to the stabilization of the TLR4 (show TLR4 Antibodies)/MD-2/metal ion complex in a conformation that enables activation.
The intensity of the intra-amniotic inflammatory response to bacteria or perhaps to other TLR4 (show TLR4 Antibodies) ligands may be facilitated through synthesis and release of sMD2 (show SNRPD2 Antibodies) by the amniochorion.
We conclude that MD2 is a significant contributor in the Ang II (show AGT Antibodies)-induced kidney inflammatory injury in chronic renal diseases.
Blockade of MD2 prevents obesity-induced inflammation and nephropathy.
MD2 is essential to obesity-related cardiac hypertrophy through activating JNK (show MAPK8 Antibodies)/ERK (show EPHB2 Antibodies) and NF-kappaB (show NFKB1 Antibodies)-dependent cardiac inflammatory pathways. Targeting MD2 would be a therapeutic approach to prevent obesity-induced cardiac injury and remodeling.
RTFs contribute to the regulation of LPS (show TLR4 Antibodies)-induced inflammatory response in RAW264.7 cells through TLR4 (show TLR4 Antibodies)/MD-2 mediated NF-kappaB (show NFKB1 Antibodies) and JNK (show MAPK8 Antibodies) pathway. It
This study provides evidence that MD2 plays a key role in the pathogenesis of retinal I/R damage.
Data suggest that C4bp prevents interaction between Tlr4 (show TLR4 Antibodies)/MD-2 and its ligand; C4bp does not appear to interact with Tlr3 (show TLR3 Antibodies); C4bp binds to macrophage surface Tlr4 (show TLR4 Antibodies) and inhibits Tlr/Tlr ligand interaction, thereby inhibiting Tlr4 (show TLR4 Antibodies) activation. (C4bp = complement component 4 binding protein; Tlr = toll (show TLR4 Antibodies)-like receptor; MD-2 = myeloid differentiation protein-2)
Oxidative stress in retinal ischemia-reperfusion injury activates TLR4 (show TLR4 Antibodies) signaling via MD2.
Neoseptin-3 and lipid A form dissimilar molecular contacts to achieve receptor activation; hence strong TLR4 (show TLR4 Antibodies)/MD-2 agonists need not mimic LPS (show TLR4 Antibodies)
Here we demonstrate that cholesterol binds to myeloid differentiation-2 (MD-2), a TLR4 (show TLR4 Antibodies) ancillary molecule.
This gene encodes a protein which associates with toll-like receptor 4 on the cell surface and confers responsiveness to lipopolysaccyaride (LPS), thus providing a link between the receptor and LPS signaling. Studies of the mouse ortholog suggest that this gene may be involved in endotoxin neutralization. Alternative splicing results in multiple transcript variants encoding different isoforms.
myeloid differentiation protein-2
, protein MD-2
, myeloid differentiation factor-2
, LPS co-receptor MD-2
, lymphocyte antigen 96
, Protein MD-2