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Results indicate that low-grade inflammation coupled with elevated blood glucose increases CD226 expression, resulting in decreased endothelial cell glucose uptake in T2DM.
Data show that the severity experimental autoimmune encephalomyelitis (EAE) were reduced and the serum IL-10 (show IL10 ELISA Kits) expression levels were increased in CD226 knockout mice than that in control mice when both received EAE induction.
Blocking CD226 inhibited NK cell-mediated cytotoxicity of the GM-CSF (show CSF2 ELISA Kits)-stimulated Flt3 ligand (show FLT3LG ELISA Kits) conventional dendritic cells. The CD226(+)NKG2A (show KLRC1 ELISA Kits)(-) subset of NK cells was better at targeting GM-CSF (show CSF2 ELISA Kits)-stimulated Flt3 ligand (show FLT3LG ELISA Kits) conventional dendritic cells. CD155 (show PVR ELISA Kits), a known ligand for CD226, could also act as an inhibitor of NK cell-mediated lysis, as dendritic cells lacking CD155 (show PVR ELISA Kits) were more sensitive to NK cell-mediated lysis.
inflammatory monocytes, together with NK cells, are essential in the early control of CMV through the DNAM-1-PVR (show PVRL2 ELISA Kits) pathway.
Data show that CD155 (show PVR ELISA Kits) protein/CD226 antigen mainly mediates the interaction between NK cells and leukemic cells in acute myeloid leukemia (show BCL11A ELISA Kits). To investigate the interaction between leukemic cells
absence of either CD155 (show PVR ELISA Kits) or CD226 in BALB/c mice causes a profound shift in the Natural Killer T-Cells subtype composition in thymus, expanding the frequency and numbers of iNKT1 cells at the expense of iNKT2 cells, as well as iNKT17 cells.
our results suggest a limited role for DNAM-1 in solid allograft rejection. Blocking DNAM-1 is not sufficient to prevent allograft rejection and might be relevant only in combination with additional inhibitors of costimulation.
we propose that expression of DNAM-1 on inflammatory monocytes are evolutionally conserved and act as an adhesion molecule (show NCAM1 ELISA Kits) on blood inflammatory monocytes.
Data indicate that DNAM-1 (CD226) signaling was required to enhance cytotoxicity.
Regulatory T cells derived (show CD4 ELISA Kits)from Cd226-deficient mice showed similarly reduced inhibitory activity, eventually resulting in an exacerbated disease course of experimental autoimmune encephalomyelitis.
Results show that CD226 expression was down-regulated in human hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) cells. MiR (show MLXIP ELISA Kits)-892a directly targeted CD226 promoting HCC (show FAM126A ELISA Kits) cells proliferation and invasion.
cumulative incidences of acute graft-versus-host disease in patients with high maximal serum levels of sDNAM-1 (>/=30 pM) in the 7 days before allogeneic hematopoietic stem cell transplantation were significantly higher than those in patients with low maximal serum levels of sDNAM-1 in the same period. Our data suggest sDNAM-1 is potentially a unique candidate as a predictive biomarker for the development of acute GVHD.
Our results support an important association of rs4810485 in CD40 (show CD40 ELISA Kits) gene and rs763361 in CD226 gene polymorphism, combined effect of rs4810485 and rs763361 with increased risk of systemic lupus erythematosus.
our results support and explain the mechanism behind the recently reported finding that in EOC, NK-cell recognition and killing of tumor cells was mainly dependent on DNAM-1 signaling while the contribution of the NKG2D (show KLRK1 ELISA Kits) receptor-ligand pathway was complementary and uncertain.
CD226 rs763361 polymorphism was significantly associated with susceptibility to T1D.
Age and CMV serostatus influence the expression of NKp30 (show NCR3 ELISA Kits), NKp46 (show NCR1 ELISA Kits) and DNAM-1 activating receptors on resting and IL-2 (show IL2 ELISA Kits) activated natural killer cells.
DNAM-1 ligands CD112 (show PVRL2 ELISA Kits) and CD155 (show PVR ELISA Kits) as well as the NKG2D (show KLRK1 ELISA Kits) ligands MICA (show MICA ELISA Kits) and MICB (show MICB ELISA Kits) were expressed on the hiPSC lines
The CD226 gene has been identified as novel association with JIA, and a SNP near CD28 (show CD28 ELISA Kits) as a suggestive association.
This gene encodes a glycoprotein expressed on the surface of NK cells, platelets, monocytes and a subset of T cells. It is a member of the Ig-superfamily containing 2 Ig-like domains of the V-set. The protein mediates cellular adhesion of platelets and megakaryocytic cells to vascular endothelial cells. The protein also plays a role in megakaryocytic cell maturation.
, CD226 molecule
, platelet and T cell activation antigen 1
, platelet and T-cell activation antigen 1
, DNAX accessory molecule 1
, DNAX accessory molecule-1
, T lineage-specific activation antigen 1 antigen
, adhesion glycoprotein