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anti-Human LY96 Anticorps:
anti-Mouse (Murine) LY96 Anticorps:
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Human Monoclonal LY96 Primary Antibody pour Func - ABIN1108191
Pugin, Stern-Voeffray, Daubeuf, Matthay, Elson, Dunn-Siegrist: Soluble MD-2 activity in plasma from patients with severe sepsis and septic shock. dans Blood 2004
Show all 4 references for ABIN1108191
Human Polyclonal LY96 Primary Antibody pour IHC (p), IHC - ABIN252602
Kunda, Cavicchia, Acosta: Lipopolysaccharides and trophic factors regulate the LPS receptor complex in nodose and trigeminal neurons. dans Neuroscience 2014
Show all 4 references for ABIN252602
Human Polyclonal LY96 Primary Antibody pour EIA, IF - ABIN500262
ONeill, Fitzgerald, Bowie: The Toll-IL-1 receptor adaptor family grows to five members. dans Trends in immunology 2003
Show all 2 references for ABIN500262
Human Monoclonal LY96 Primary Antibody pour Func, EIA - ABIN1108192
Viriyakosol, McCray, Ashbaugh, Chu, Jia, Weiss, Kirkland: Characterization of monoclonal antibodies to human soluble MD-2 protein. dans Hybridoma (2005) 2007
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 (Montrer PPP3R1 Anticorps) 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 (Montrer TLR4 Anticorps)/MD2 complex together with the co-receptor CD14 (Montrer NDUFA2 Anticorps)
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 (Montrer TLR4 Anticorps) signaling.
Predominantly hydrophobic interactions between MD-2 and TLR4 (Montrer TLR4 Anticorps) contribute to the stabilization of the TLR4 (Montrer TLR4 Anticorps)/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 (Montrer TLR4 Anticorps) ligands may be facilitated through synthesis and release of sMD2 (Montrer SNRPD2 Anticorps) by the amniochorion.
Three genes (LY96, IL8 (Montrer IL8 Anticorps) DPR (Montrer DACT1 Anticorps)) 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 (Montrer TLR4 Anticorps).
Gene polymorphisms of MD2 and GM2A (Montrer GM2A Anticorps) 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.
Oxidative stress in retinal ischemia-reperfusion injury activates TLR4 (Montrer TLR4 Anticorps) signaling via MD2.
Neoseptin-3 and lipid A form dissimilar molecular contacts to achieve receptor activation; hence strong TLR4 (Montrer TLR4 Anticorps)/MD-2 agonists need not mimic LPS (Montrer TLR4 Anticorps)
Here we demonstrate that cholesterol binds to myeloid differentiation-2 (MD-2), a TLR4 (Montrer TLR4 Anticorps) ancillary molecule.
MD-2 is a critical regulator of the establishment of allergic airway sensitization to HDM (Montrer HDAC3 Anticorps) 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 (Montrer SSRP1 Anticorps) (HMGB1 (Montrer HMGB1 Anticorps)) to facilitate toll-like receptor 4 (TLR4 (Montrer TLR4 Anticorps))-dependent signaling.
Carbon monoxide treatment reduces the expression of the TLR4 (Montrer TLR4 Anticorps)/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 (Montrer PITX3 Anticorps)-opsonized Aspergillus conidia activated the TLR4/Toll (Montrer TLR4 Anticorps)/IL-1R domain-containing adapter inducing IFN-beta (Montrer IFNB1 Anticorps)-dependent signaling pathway converging on IL-10 (Montrer IL10 Anticorps).
SAA3 directly binds MD-2 and activates the MyD88 (Montrer MYD88 Anticorps)-dependent TLR4 (Montrer TLR4 Anticorps)/MD-2 pathway.
Monophosphoryl lipid A is unable to efficiently form TLR4 (Montrer TLR4 Anticorps)/MD-2 heterotetramers, but it still needs heterotetramer formation for the full extent of signaling it is able to achieve.
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