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Human LY96 Protein expressed in HEK-293 Cells - ABIN2725664
Dulay, Buhimschi, Zhao, Oliver, Abdel-Razeq, Shook, Bahtiyar, Buhimschi: Amniotic Fluid Soluble Myeloid Differentiation-2 (sMD-2) as Regulator of Intra-amniotic Inflammation in Infection-induced Preterm Birth. in American journal of reproductive immunology (New York, N.Y. : 1989) 2015
MD-2 siRNA or plasmid further confirmed the efficacy of Iturin A by suppressing MD-2/TLR4 (show TLR4 Proteins) signaling pathway. The in silico docking study showed that the Iturin A interacted well with the MD-2 in MD-2/TLR4 (show TLR4 Proteins) receptor complex. Conclusively, inhibition of MD-2/TLR4 (show TLR4 Proteins) complex with Iturin A offered strategic advancement in cancer therapy.
data confirm that engineered human cells expressing TLR4 (show TLR4 Proteins), MD2 and CD14 (show NDUFA2 Proteins) can respond to CMP (show MATN1 Proteins) with NF-kappaB (show NFKB1 Proteins) activation and the response can be influenced by variations in CMP (show MATN1 Proteins)-mannosylation
The observations suggest that MD-2 helps to regulate lipopolysaccharide-induced NLRP3 (show NLRP3 Proteins) inflammasome activation and the inflammatory response in NR8383 cells, and likely does so by affecting MyD88 (show MYD88 Proteins)/NF-kappaB (show NFKB1 Proteins) 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 Proteins) 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 Proteins)/MD2 complex together with the co-receptor CD14 (show NDUFA2 Proteins)
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 Proteins) signaling.
Predominantly hydrophobic interactions between MD-2 and TLR4 (show TLR4 Proteins) contribute to the stabilization of the TLR4 (show TLR4 Proteins)/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 Proteins) ligands may be facilitated through synthesis and release of sMD2 (show SNRPD2 Proteins) by the amniochorion.
Three genes (LY96, IL8 (show IL8 Proteins) DPR (show DACT1 Proteins)) were significantly downregulated over time. This finding was confirmed in a validation cohort of stroke patients (n=8).
MD2 is essential to obesity-related cardiac hypertrophy through activating JNK (show MAPK8 Proteins)/ERK (show EPHB2 Proteins) and NF-kappaB (show NFKB1 Proteins)-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 Proteins)-induced inflammatory response in RAW264.7 cells through TLR4 (show TLR4 Proteins)/MD-2 mediated NF-kappaB (show NFKB1 Proteins) and JNK (show MAPK8 Proteins) 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 Proteins)/MD-2 and its ligand; C4bp does not appear to interact with Tlr3 (show TLR3 Proteins); C4bp binds to macrophage surface Tlr4 (show TLR4 Proteins) and inhibits Tlr/Tlr ligand interaction, thereby inhibiting Tlr4 (show TLR4 Proteins) activation. (C4bp = complement component 4 binding protein; Tlr = toll (show TLR4 Proteins)-like receptor; MD-2 = myeloid differentiation protein-2)
Oxidative stress in retinal ischemia-reperfusion injury activates TLR4 (show TLR4 Proteins) signaling via MD2.
Neoseptin-3 and lipid A form dissimilar molecular contacts to achieve receptor activation; hence strong TLR4 (show TLR4 Proteins)/MD-2 agonists need not mimic LPS (show TLR4 Proteins)
Here we demonstrate that cholesterol binds to myeloid differentiation-2 (MD-2), a TLR4 (show TLR4 Proteins) ancillary molecule.
MD-2 is a critical regulator of the establishment of allergic airway sensitization to HDM (show HDAC3 Proteins) 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 Proteins) (HMGB1 (show HMGB1 Proteins)) to facilitate toll-like receptor 4 (TLR4 (show TLR4 Proteins))-dependent signaling.
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