United States set
language
Menu Shopping cart $0 Search
Manufactured by BioVendor

sE-Selectin Human ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, HRP-labelled antibody
  • Species:Human
Cat. No. Size Price


RAF098R 96 wells (1 kit) $721,83
PubMed Product Details
Technical Data

Type

Sandwich ELISA, HRP-labelled antibody

Applications

Serum, Plasma, Cell culture supernatant

Sample Requirements

20 µl/well

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

1.6–50 ng/ml

Limit of Detection

0.3 ng/ml

Intra-assay (Within-Run)

CV = 5.4%

Inter-assay (Run-to-Run)

CV = 6.0%

Spiking Recovery

86,00%

Dilution Linearity

95,00%

Summary

Research topic

Cell adhesion proteins

Summary

Endothelial Leukocyte Adhesion Molecule-1 (ELAM-1, E-selectin) belongs to the selectin family of adhesion molecules. Together with LECAM-1 (L-selectin) and GMP-140 (P-selectin), Eselectin mediates the initial interactions of leukocytes and platelets with endothelial cells. Molecular structure: The extracellular part of all selectins consists of an aminoterminal c-type lectin domain which specifically binds to carbohydrate ligands. This is followed by an EGF-like domain, and, in the case of E-selectin, by 6 short consensus repeats. The transmembrane portion of the molecule is followed by a short cytoplasmic tail. Selectins guide non-activated polymorphonuclear cells to the areas of inflammation in creating first, loose contacts with the endothelial layer. The potential binding partner of E-selectin contains sialyl LewisX oligosaccharide. Other suitable ligands for the lectin domain of Eselectin are sialylated, fucosylated lactosaminoglycans. Together with GMP-140, E-selectin
is expressed on cytokine-activated endothelial cells, and contributes to the adhesion of still resting leukocytes to the endothelium. This initial binding event is an essential prerequisite for the activation of the immune cells via different inflammatory mediators. In contrast to GMP- 140, E-selectin is maximally expressed 2-4 hours after cell activation. Within the next 24-48 hours E-selectin is again eliminated from the cytoplasmic membrane by shedding into the circulation. The circulating form or soluble (sE-selectin) of this selectin exerts chemotactical signals on neutrophils and additionally activates the 2-integrins - sE-selectin assists in preparing the migration capacity of these cells. Determination of sE-selectin could provide more detailed insights into the pathological
modifications during various diseases:

  • Allergic reactions: The transient influx of neutrophils into the respiratory tract, due to an inflammatory response is predominantly mediated via E-selectin. A functional role for this molecule in the development of acute airway inflammation in vivo has been demonstrated. Additionally, E-selectin may be of particular importance for the start phase of allergic contact dermatitis.
  • Ocular diseases: The presents of E-selectin on retinal vascular endothelium suggests an important role for this selectin in the pathogenesis of immunologically mediated ocular conditions.
  • Septic shock: E-selectin seems to be involved in the pathogenesis of "multiple organ failure (MOF)" during septic shock.
  • Vascular infection and inflammation: The levels of sE-selectin in patients with a recent onset of giant cell arteriitis or polyarteriitis nodosa are significantly higher than in normal controls.
  • Inflammatory bowel disease: E-selectin is expressed on colonic endothelial surfaces in association with inflammation.
  • Transplantation: Increased E-selectin expression on endothelial cells is found in graft-versushost-disease.
Product References (1)

References

  • Manco M, Nobili V, Alisi A, Panera N, Handberg A. Arterial Stiffness, Thickness and Association to Suitable Novel Markers of Risk at the Origin of Cardiovascular Disease in Obese Children. Int J Med Sci. 2017 Jul 12;14(8):711-720. doi: 10.7150/ijms.20126. eCollection 2017. PubMed PMID: 28824305. PubMed CentralPMCID: PMC5562124. See more on PubMed
Summary References (18)

References to Selectin

  • Buhrer C, Luxenburger U, Metze B, Kattner E, Henze G, Dudenhausen JW, Obladen M. Diminished cord blood lymphocyte L-selectin expression in neonatal bacterial infection. Eur J Pediatr. 1993 Jun;152 (6):519-22
  • Finn A, Moat N, Rebuck N, Klein N, Strobel S, Elliott M. Changes in neutrophil CD11b/CD18 and L-selectin expression and release of interleukin 8 and elastase in paediatric cardiopulmonary bypass. Agents Actions. 1993;38 Spec No:C44-6
  • Foxall C, Watson SR, Dowbenko D, Fennie C, Lasky LA, Kiso M, Hasegawa A, Asa D, Brandley BK. The three members of the selectin receptor family recognize a common carbohydrate epitope, the sialyl Lewis(x) oligosaccharide. J Cell Biol. 1992 May;117 (4):895-902
  • Hogg N. Roll, roll, roll your leucocyte gently down the vein.... Immunol Today. 1992 Apr;13 (4):113-5
  • Jutila MA, Kishimoto TK, Finken M. Low-dose chymotrypsin treatment inhibits neutrophil migration into sites of inflammation in vivo: effects on Mac-1 and MEL-14 adhesion protein expression and function. Cell Immunol. 1991 Jan;132 (1):201-14
  • Kishimoto TK, Jutila MA, Berg EL, Butcher EC. Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors. Science. 1989 Sep 15;245 (4923):1238-41
  • Klein NJ, Levin M, Strobel S, Finn A. Degradation of glycosaminoglycans and fibronectin on endotoxin-stimulated endothelium by adherent neutrophils: relationship to CD11b/CD18 and L-selectin expression. J Infect Dis. 1993 Apr;167 (4):890-8
  • Lampeter ER, Kishimoto TK, Rothlein R, Mainolfi EA, Bertrams J, Kolb H, Martin S. Elevated levels of circulating adhesion molecules in IDDM patients and in subjects at risk for IDDM. Diabetes. 1992 Dec;41 (12):1668-71
  • Lasky LA. Lectin cell adhesion molecules (LEC-CAMs): a new family of cell adhesion proteins involved with inflammation. J Cell Biochem. 1991 Feb;45 (2):139-46
  • Mengelers HJ, Maikoe T, Hooibrink B, Kuypers TW, Kreukniet J, Lammers JW, Koenderman L. Down modulation of L-Selectin expression on eosinophils recovered from bronchoalveolar lavage fluid after allergen provocation. Clin Exp Allergy. 1993 Mar;23 (3):196-204
  • Moller P, Eichelmann A, Leithauser F, Mechtersheimer G, Otto HF. Venular endothelium binding molecules CD44 and LECAM-1 in normal and malignant B-cell populations. A comparative study. Virchows Arch A Pathol Anat Hi. 1992;421 (4):305-13
  • Schleiffenbaum B, Spertini O, Tedder TF. Soluble L-selectin is present in human plasma at high levels and retains functional activity. J Cell Biol. 1992 Oct;119 (1):229-38
  • Smith CW, Kishimoto TK, Abbassi O, Hughes B, Rothlein R, McIntire LV, Butcher E, Anderson DC. Chemotactic factors regulate lectin adhesion molecule 1 (LECAM-1)-dependent neutrophil adhesion to cytokine-stimulated endothelial cells in vitro. J Clin Invest. 1991 Feb;87 (2):609-18
  • Spertini O, Schleiffenbaum B, White-Owen C, Ruiz P Jr, Tedder TF. ELISA for quantitation of L-selectin shed from leukocytes in vivo. J Immunol Methods. 1992 Nov 25;156 (1):115-23
  • Stewart GJ. Neutrophils and deep venous thrombosis. Haemostasis. 1993 Mar;23 Suppl 1:127-40
  • Tozeren A, Ley K. How do selectins mediate leukocyte rolling in venules?. Biophys J. 1992 Sep;63 (3):700-9
  • Von Andrian UH, Hansell P, Chambers JD, Berger EM, Torres Filho I, Butcher EC, Arfors KE. L-selectin function is required for beta 2-integrin-mediated neutrophil adhesion at physiological shear rates in vivo. Am J Physiol. 1992 Oct;263 (4 Pt 2):H1034-44
  • Zimmerman GA, Prescott SM, McIntyre TM. Endothelial cell interactions with granulocytes: tethering and signaling molecules. Immunol Today. 1992 Mar;13 (3):93-100
Related Products Docs