产品名称 Mouse SELE Antibody from CREATIVE DIAGNOSTICS
产品货号 CABT-L293
产品价格 现货询价,电话:010-67529703
产品规格 n/a
产品品牌 CREATIVE DIAGNOSTICS
产品概述
产品详情
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Antigenic SpecificityMouse SELE
Clone7520
Host SpeciesRat
Reactive Speciesmouse
IsotypeIgG1
Formatunconjugated
Sizen/a
Concentrationn/a
ApplicationsELISA(Cap), WB
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DescriptionRat Anti-Mouse SELE monoclonal antibody for ELISA(Cap), WB. E-Selectin (Endothelial Leukocyte Adhesion Molecule-1, ELAM-1, CD62E), a member of the Selectin family, is a 107-115 kDa cell surface glycoprotein. It is transiently expressed on vascular endothelial cells in response to IL-1 beta b and TNF-alpha, and demonstrates peak expression at 4 hours, and decay at 24 hours, in response to activation. E-Selectin ligands, expressed on neutrophils, monocytes, and a subset of memory T cells, are sialylated, fucosylated molecules which bind to the lectin domain of E-Selectin. Immunocytochemical techniques have demonstrated the expression of E-Selectin on healthy and diseased tissue. The human and mouse E-Selectin proteins share 81% amino acid similarity.E-Selectin mediates the attachment of flowing leukocytes to the blood vessel wall during inflammation by binding to E-Selectin ligands on leukocytes. These interactions are labile and permit leukocytes to roll along the vascular endothelium in the direction of blood flow. This initial interaction is followed by a stronger interaction involving ICAM-1 and VCAM-1 that leads eventually to extravasation of the white blood cell through the blood vessel wall into the extracellular matrix tissue.ELISA techniques have shown that detectable levels of soluble E-Selectin are present in the biological fluids of apparently normal individuals. Furthermore, a number of studies have reported that levels of E-Selectin may be elevated in subjects with a variety of pathological conditions.
ImmunogenRecombinant Protein
Other Namesn/a
Gene, Accession #Gene ID: 20339, UniProt: Q00690
Catalog #CABT-L293
Price
Order / More InfoMouse SELE Antibody from CREATIVE DIAGNOSTICS
Product Specific Referencesn/a
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