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anti-Human LY96 Antibodies:
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Human Monoclonal LY96 Primary Antibody for Func - ABIN1108191
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
Show all 4 references for ABIN1108191
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
Show all 3 references for ABIN252602
Human Polyclonal LY96 Primary Antibody for EIA, IF - ABIN500262
ONeill, Fitzgerald, Bowie: The Toll-IL-1 receptor adaptor family grows to five members. in Trends in immunology 2003
Show all 2 references for ABIN500262
Human Monoclonal LY96 Primary Antibody for Func, EIA - ABIN1108192
Viriyakosol, McCray, Ashbaugh, Chu, Jia, Weiss, Kirkland: Characterization of monoclonal antibodies to human soluble MD-2 protein. in Hybridoma (2005) 2007
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.
Three genes (LY96, IL8 (show IL8 Antibodies) DPR (show DACT1 Antibodies)) were significantly downregulated over time. This finding was confirmed in a validation cohort of stroke patients (n=8).
The study revealed the impact of specific residues and regions of MD-2 on the binding of lipolysaccharides and TLR4 (show TLR4 Antibodies).
Gene polymorphisms of MD2 and GM2A (show GM2A Antibodies) were associated with the occurrence or severity of neonatal necrotizing enterocolitis.
In patients undergoing CABG surgery, we found genetic polymorphisms in LY96 associated with decreased risk of postoperative AF.
Aminoarabinose residues in lipid A contribute to Burkholderia lipid A binding to the TLR4 (show TLR4 Antibodies).Myeloid Differentiation Factor 2 complex.
TLR4 (show TLR4 Antibodies) 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)
In monocytes of sepsis, MD-2 expression was found to be regulated by STAT1 (show STAT1 Antibodies).
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.
MD-2 is a critical regulator of the establishment of allergic airway sensitization to HDM (show HDAC3 Antibodies) in mice. Serum MD-2 may represent a potential biomarker for the amplification of allergic sensitization and allergic inflammation.
Data show that myeloid differentiation factor 2 (MD-2) binds specifically to disulfide isoform of box protein 1, high mobility group (show SSRP1 Antibodies) (HMGB1 (show HMGB1 Antibodies)) to facilitate toll-like receptor 4 (TLR4 (show TLR4 Antibodies))-dependent signaling.
Carbon monoxide treatment reduces the expression of the TLR4 (show TLR4 Antibodies)/MD2 complex on the surface of myeloid cells, which renders them resistant to lipopolysaccharide priming in vitro, as well as in vivo in a model of endotoxic shock.
Mechanistically, engagement of MD-2 by PTX3 (show PITX3 Antibodies)-opsonized Aspergillus conidia activated the TLR4/Toll (show TLR4 Antibodies)/IL-1R domain-containing adapter inducing IFN-beta (show IFNB1 Antibodies)-dependent signaling pathway converging on IL-10 (show IL10 Antibodies).
SAA3 directly binds MD-2 and activates the MyD88 (show MYD88 Antibodies)-dependent TLR4 (show TLR4 Antibodies)/MD-2 pathway.
Monophosphoryl lipid A is unable to efficiently form TLR4 (show TLR4 Antibodies)/MD-2 heterotetramers, but it still needs heterotetramer formation for the full extent of signaling it is able to achieve.
Data show that rifampin binds to myeloid differentiation protein 2 (MD-2), the key coreceptor for innate immune TLR4 (show TLR4 Antibodies).
Gb4 is an endogenous ligand for TLR4 (show TLR4 Antibodies)-MD-2 and is capable of attenuating LPS (show TLR4 Antibodies) toxicity, indicating the possibility for its therapeutic application in endotoxin shock.
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