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Human Selectin E + CD62e Protein expressed in Human Cells - ABIN2002601
Phillips, Nudelman, Gaeta, Perez, Singhal, Hakomori, Paulson: ELAM-1 mediates cell adhesion by recognition of a carbohydrate ligand, sialyl-Lex. in Science (New York, N.Y.) 1991
Show all 6 Pubmed References
additive expression of RUNX1 in HUVECs resulted in the upregulation of E-selectin
Results highlight novel mechanisms by which p38 downregulates the expression of E-selectin through miR-146a and miR-31 following inflammatory stimuli associated to cancer progression.
Levels of E and P selectin showed positive correlation with the length of stay.
Our study shows a significant association of E-selectin gene polymorphism(Leu554Phe) with essential hypertension.
The highest levels of sL- and sE-selectin were observed in colorectal patients with lymph node metastasis.
Circulating CD62E(+) microparticle levels are abnormal in subjects with pre-diabetes.
sVCAM-1 reflects xerostomia in primary Sjogren's syndrome. sICAM-1 and sE-selectin may be additional parameters of secondary Sjogren's syndrome activity.
Neutrophil rolling over E-selectin at precise shear stress transmits tension and catch-bond formation with L-selectin via sLe(x), resulting in focal clusters that deliver a distinct signal to upshift beta2-integrins to a high-affinity state. Rivipansel effectively blocked formation of selectin catch-bonds, revealing a novel mechanotransduction circuit
E-selectin-dependent rolling promotes adhesion to HA by both physically slowing cells and enabling them to position proximal to the surface, thereby increasing the on rate of adhesion.
High E-selectin expression is associated with breast cancer metastasis.
his study shows that two adhesion molecules, shed as soluble forms, are elevated during the acute phase of leptospirosis: E-selectin and s-ICAM1. These molecules may interfere with the process of immune cell recruitment to clear Leptospira at tissue levels.
ELAM-1 upregulation may promote disorder in adhesion, and migration of the cells leading to the endometriosis disorder.
Elevated endothelium-related mediators (vWF, E-selectin and EPCR) appear to participate in the development of pancreatic necrosis and may be a potential indicator of overall prognosis.
interplay between flow-dependent on-rate and off-rate of E-selectin-ligand bonds determine flow-enhanced cell rolling stability
High SELE expression is associated with Inflamed Atherosclerotic Plaque.
In this study, we addressed this question by analysing sLex expression together with two glycoproteins (BST-2 and LGALS3BP), shown to interact with E-selectin in a carbohydrate-dependent manner, in a cohort of 249 invasive breast cancers
SELE expression is significantly upregulated in human masticatory mucosa during wound healing
E-selectin concentrations in this study were associated with hyperglycemia, possibly reflecting early endothelial damage. E-selectin was not useful to assess carotid intima-media thickness, a marker of subclinical atherosclerosis, which appeared to be determined by aging and male gender.
Plasma E-selectin is overexpressed in pediatric patients with mycoplasma pneumoniae pneumonia and myocardial injury.
The significant presence of CLA+ T cells and E-selectin (CD62E) expressions in the OLPG suggests their involvement in the etiopathogenesis of oral lichen planus ; however, only a weak correlation between CLA+ T cells and E-selectin was observed.
Chitosan oligosaccharides downregulate the expression of E-selectin and ICAM-1 by inhibiting the phosphorylation of Mitogen-Activated Protein Kinases and the activation of NF-kappaB in lipopolysaccharides treated porcine iliac artery endothelial cells.
Increased E-selectin mRNA at end of 20 hours of cold ischemia time might indicate a preactivated state of endothelial cells potentially triggered by bacterial translocation or products.
The e-selectin/biliverdin reductase pathway participates in the inhibitory process of hypoxia in pulmonary artery endothelial cell apoptosis which is mediated by the mitochondrial-dependent apoptosis pathway.
Five single nucleotide polymorphisms (SNPs) from different exons in selectin SELP, two in selectin SELL and one in selectin SELE were taken forward to genotyping in 337 Holstein Friesian heifers using PCR-RFLP.
Study reports that stromal cell-derived factor-1alpha elevated or therapeutically administered in ischemic wounded tissue can stimulate both local endothelial cells (EC) and bone marrow-derived endothelial progenitor cells (EPC) to express reciprocally E-selectin/ligand pairs and thereby enhance EPC-EC interactions.
Before the arrival of tumor cells, the lung-recruited monocytic myeloid-derived suppressor cells produced IL-1beta, thereby increasing E-selectin expression and promoting tumor cell arrest on endothelial cells.
Inhibiting E-selectin attenuated inflammation in atherosclerotic plaques, likely by reducing leukocyte recruitment into plaques and by mitigating hematopoietic stem and progenitor cell activation in the spleen of mice with myocardial infarction.
In a model of corneal transplantation, P- and E-selectin mediate T cell recruitment to the graft, E-selectin mediates APC trafficking to lymphoid tissue, and blockade of E-selectin has a modest effect on improving long-term graft survival.
Social defeat induced an exposure-dependent increase in mRNA levels of E-selectin, CXCL1, and CXCL2 that increased with additional days of social defeat.
Complex spatiotemporal expression dynamics of selectins determine the sequential extravasation of neutrophils and inflammatory monocytes in the acute inflammatory response.
involved in neutrophil recruitment into the kidney after induction of sepsis
The histopathological modification of lupus nephritis by non-nephritogenic bystander IgM antibodies is associated in part with glomerular E-selectin expression.
Data show that actin cytoskeleton regulated CD44 membrane mobility and interactions with E-selectin.
Regulatory T cells dynamically regulate P and E selectin ligand expression during multiple challenge contact hypersensitivity.
Systemic inflammation may increase the expression of E-selectin which mediated the lung metastasis of breast cancer in mouse model.
In the absence of either PSGL-1 or E- and P-selectin.
The study suggest that E- and P-selectins play an important role in leukemic dissemination in chronic myelogenous and chronic eosinophilic leukemias.
Elevated E-selectin plays an important role in hepatic neutrophil infiltration and injury induced by chronic-binge feeding in mice and may also contribute to the pathogenesis of early stages of human alcoholic liver disease.
expression of E-selectin and ICAM-1 are suppressed by paeoniflorin in a mouse model of cutaneous Arthus reaction
Expression of E-selectin is sufficient to support rescue & hematopoietic reconstitution of lethally irradiated recipients forllowing bone marrow transplant.
TWEAK acted as an inducer of E-selectin and ICAM-1 expression in mice with cutaneous vasculitis and human dermal microvascular endothelial cells
E-selectin deficiency presents a protective effect on cerebral ischemia, likely achieved by the inhibition of inflammation and apoptosis.
Constitutively expressed E-selectin on endothelial cells in the proliferating phase is one mediator of the stem cell tropism in infantile hemangioma.
beta(3)-adrenergic stimulation acts through up-regulation of E-selectin in adipose tissue endothelial cells to induce neutrophil infiltration
The protein encoded by this gene is found in cytokine-stimulated endothelial cells and is thought to be responsible for the accumulation of blood leukocytes at sites of inflammation by mediating the adhesion of cells to the vascular lining. It exhibits structural features such as the presence of lectin- and EGF-like domains followed by short consensus repeat (SCR) domains that contain 6 conserved cysteine residues. These proteins are part of the selectin family of cell adhesion molecules. Adhesion molecules participate in the interaction between leukocytes and the endothelium and appear to be involved in the pathogenesis of atherosclerosis.
, endothelial adhesion molecule 1
, selectin E (endothelial adhesion molecule 1)
, CD62 antigen-like family member E
, endothelial leukocyte adhesion molecule 1
, leukocyte endothelial cell adhesion molecule 2
, leukocyte-endothelial cell adhesion molecule 2
, selectin, endothelial cell