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anti-Mouse (Murine) CD226 Anticorps:
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Human Monoclonal CD226 Primary Antibody pour FACS - ABIN4896040
Brunetta, Fogli, Varchetta, Bozzo, Hudspeth, Marcenaro, Moretta, Mavilio: The decreased expression of Siglec-7 represents an early marker of dysfunctional natural killer-cell subsets associated with high levels of HIV-1 viremia. dans Blood 2009
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Human Monoclonal CD226 Primary Antibody pour FACS - ABIN4896039
Liu, Qian, Chen, Xu, Gao, Zhang, Zhang, Qi, Gao, Yan: Crystal structure of cell adhesion molecule nectin-2/CD112 and its binding to immune receptor DNAM-1/CD226. dans Journal of immunology (Baltimore, Md. : 1950) 2012
Human Monoclonal CD226 Primary Antibody pour CyTOF, FACS - ABIN4899392
Magnani, Alberigo, Bacchetta, Serafini, Andreani, Roncarolo, Gregori: Killing of myeloid APCs via HLA class I, CD2 and CD226 defines a novel mechanism of suppression by human Tr1 cells. dans European journal of immunology 2011
Human Monoclonal CD226 Primary Antibody pour FACS - ABIN2689098
Shibuya, Campbell, Hannum, Yssel, Franz-Bacon, McClanahan, Kitamura, Nicholl, Sutherland, Lanier, Phillips: DNAM-1, a novel adhesion molecule involved in the cytolytic function of T lymphocytes. dans Immunity 1996
Human Monoclonal CD226 Primary Antibody pour FACS, IP - ABIN2479326
Fretz, Stark, Metz, Elizondo, Weissleder, Shen, Wittenberg, Simeone, Ferrucci: Detection of hepatic metastases: comparison of contrast-enhanced CT, unenhanced MR imaging, and iron oxide-enhanced MR imaging. dans AJR. American journal of roentgenology 1990
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Human Monoclonal CD226 Primary Antibody pour FACS - ABIN2479327
Shibuya, Lanier, Phillips: Protein kinase C is involved in the regulation of both signaling and adhesion mediated by DNAX accessory molecule-1 receptor. dans Journal of immunology (Baltimore, Md. : 1950) 1998
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Human Monoclonal CD226 Primary Antibody pour Func, FACS - ABIN2479328
Kojima, Kanada, Shimizu, Kasama, Shibuya, Nakauchi, Nagasawa, Shibuya: CD226 mediates platelet and megakaryocytic cell adhesion to vascular endothelial cells. dans The Journal of biological chemistry 2003
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This study clarifies how DNAM-1 modifies the bidirectional crosstalk of natural killer cells with CD155(+) dendritic cells, which can be exploited to suppress CNS autoimmunity and strengthen tumor surveillance
CD226 is involved in megakaryocyte activation and early-stage differentiation.
The hybrid complex structure of CD226-ecto binding to the first domain of CD155 (hCD155-D1) reveals a conserved binding interface with the first domain of CD226 (D1), whereas the second domain of CD226 (D2) both provides structural supports for the unique architecture of CD226 and forms direct interactions with CD155.
CD226 regulation of NK cell cytotoxicity is facilitated through inactivation of FOXO1. Gene-expression analysis of NK cells isolated from syngeneic tumors grown in wild-type or CD226-deficient mice revealed dysregulated expression of FOXO1-regulated genes in the absence of CD226.
DNAM-1 (CD226) has been associated with specific inhibitory receptors, suggesting that it might be functionally involved in natural killer cell education. The present study shows that DNAM-1 function is associated with natural killer cell education but is not necessary to reach nor maintain the educated state. The authors propose a model in which natural killer cell education prevents or delays downregulation of DNAM-1.
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 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-stimulated Flt3 ligand conventional dendritic cells. The CD226(+)NKG2A(-) subset of NK cells was better at targeting GM-CSF-stimulated Flt3 ligand conventional dendritic cells. CD155, a known ligand for CD226, could also act as an inhibitor of NK cell-mediated lysis, as dendritic cells lacking CD155 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 pathway.
Data show that CD155 protein/CD226 antigen mainly mediates the interaction between NK cells and leukemic cells in acute myeloid leukemia. To investigate the interaction between leukemic cells
absence of either CD155 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 on blood inflammatory monocytes.
Data indicate that DNAM-1 (CD226) signaling was required to enhance cytotoxicity.
Regulatory T cells derived from Cd226-deficient mice showed similarly reduced inhibitory activity, eventually resulting in an exacerbated disease course of experimental autoimmune encephalomyelitis.
CD226 limits spontaneous multiple myeloma development in Vk*MYC transgenic mice. This is mediated both by NK and CD8+ T cells through perforin and IFN-gamma pathways. It also is needed for cyclophosphamide and bortezomib treatment effectiveness.
Findings suggest that TIGIT is a key checkpoint inhibitor of chronic antiviral and antitumor responses through impairing CD226 function when disrupting its homodimerization.
This synapse defect may explain why DNAM-1-deficient mice cannot clear tumors in vivo.
cooperative signaling through DNAM-1 and Ly49H are required for NK cell-mediated host defense against MCMV infection
An inactivation gene strategy showed that DNAM-1 exerts profibrotic effects by controlling T cell activation and cytokine release.
this study shows that NK cells lyse Th2-polarizing dendritic cells via DNAM1
Our study did not show significant association of CD226 and CD247 genetic polymorphisms with the risk of SSc or the presence of clinical manifestations except than FVC. In other words, CD226 and CD247 genetic variants may not contribute to SSc pathogenesis in Iranian population.
this paper shows that the decreased expression of activating receptor DNAM-1 on peripheral blood NK cells is positively associated with gastric cancer progression
T allele and TT genotype of the CD226 rs763361 polymorphism is associated with susceptibility to type 1 diabetes and with a lower age of disease onset among Egyptian children
These findings highlight the importance of the TIGIT/CD226/PVR axis as an immune checkpoint barrier that could hinder future "cure" strategies requiring potent HIV-specific CD8(+) T cells
Sole engagement of NKG2D, 2B4 or DNAM-1 is insufficient for NF-kappaB activation.
The Serum level of CD226 and not CD226 genotypes could be considered as an independent risk factor for the prediction of RA within healthy individuals and also for RA disease activity.
Natural killer cells and cytotoxic T cells express both TIGIT and DNAM-1 receptors, and in certain cases their effector functions are dictated by TIGIT or DNAM-1 signaling. Agonist and antagonist antibodies targeting either TIGIT or DNAM-1 present many therapeutic options for diseases spanning from cancer to auto-immunity. (Review)
Results show that CD226 expression was down-regulated in human hepatocellular carcinoma (HCC) cells. MiR-892a directly targeted CD226 promoting HCC 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 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 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, NKp46 and DNAM-1 activating receptors on resting and IL-2 activated natural killer cells.
DNAM-1 ligands CD112 and CD155 as well as the NKG2D ligands MICA and MICB were expressed on the hiPSC lines
The CD226 gene has been identified as novel association with JIA, and a SNP near CD28 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