InVivoMAb anti-human E-Selectin

Clone Catalog # Category
CL2 BE0136 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-human E-Selectin

The CL2 monoclonal antibody reacts with human E-selectin also known as CD62E, endothelial-leukocyte adhesion molecule 1 (ELAM-1), and leukocyte-endothelial cell adhesion molecule 2 (LECAM2). E-selectin is a 115 kDa type I transmembrane protein and a member of the selectin family of adhesion molecules. E-selectin is expressed on cytokine-activated endothelial cells. Along with L-selectin and P-selectin, E-selectin mediates the initial interactions of leukocytes and platelets with endothelial cells. E-selectin is thought to play a role in inflammation, tumor metastasis, and angiogenesis. The CL2 antibody has been shown to inhibit neutrophil adhesion to E-selectin and to P-selectin.

InVivoMAb anti-human E-Selectin Specifications

Isotype

Mouse IgG2a, κ

Recommended Isotype Control(s) InVivoMAb mouse IgG2a isotype control, unknown specificity(BE0085)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

Not available or unknown

Reported Applications

Flow cytometry

Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Sterility

0.2 μM filtered

Production

Purified from tissue culture supernatant in an animal free facility

Purification

Protein G

Storage

The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

RRID

AB_10949619

Molecular Weight

150 kDa

Application References

InVivoMAb anti-human E-Selectin (Clone: CL2)

  Goncharova, V., et al. (2014). "Homing of neural stem cells from the venous compartment into a brain infarct does not involve conventional interactions with vascular endothelium." Stem Cells Transl Med 3(2): 229-240. PubMed

Human neural stem cells (hNSCs) hold great potential for treatment of a wide variety of neurodegenerative and neurotraumatic conditions. Heretofore, administration has been through intracranial injection or implantation of cells. Because neural stem cells are capable of migrating to the injured brain from the intravascular space, it seemed feasible to administer them intravenously if their ability to circumvent the blood-brain barrier was enhanced. In the present studies, we found that interactions of hNSCs in vitro on the luminal surface of human umbilical vein endothelial cells was enhanced following enforced expression of cutaneous lymphocyte antigen on cell surface moieties by incubation of hNSCs with fucosyltransferase VI and GDP-fucose (fhNSCs). Interestingly, ex vivo fucosylation of hNSCs not only did not improve the cells homing into the brain injured by stroke following intravenous administration but also increased mortality of rats compared with the nonfucosylated hNSC group. Efforts to explain these unexpected findings using a three-dimensional flow chamber device revealed that transmigration of fhNSCs (under conditions of physiological shear stress) mediated by stromal cell-derived factor 1alpha was significantly decreased compared with controls. Further analysis revealed that hNSCs poorly withstand physiological shear stress, and their ability is further decreased following fucosylation. In addition, fhNSCs demonstrated a higher frequency of cellular aggregate formation as well as a tendency for removal of fucose from the cell surface. In summary, our findings suggest that the behavior of hNSCs in circulation is different from that observed with other cell types and that, at least for stroke, intravenous administration is a suboptimal route, even when the in vitro rolling ability of hNSCs is optimized by enforced fucosylation.

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