Data sheet
| Size | 100ug/vial |
| Storage | At -20C for one year. After reconstitution, at 4C for one month. |
| Form | lyophilized |
| Ig type | rabbit IgG |
| Immunogen/Antigen | A synthetic peptide corresponding to a sequence at the N-terminal |
| Reconstitution | 0.2ml of distilled water will yield a concentration of 500μg/ml. |
More info
Background
E-Selectin(SELE), also called Selectin E, ELAM1 or ELAM, is a cell adhesion molecule expressed only on endothelial cells activated by cytokines. It 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. E-Selection is a member of the selectin family of cell adhesion molecules. The E-Selectin gene is mapped on 1q24.2. The ELAM gene is present in single copy in the human genome and contains 14 exons spanning about 13 kb of DNA by Collins et al. Using affinity chromatography, pull-down assays, and mass spectrometric analysis on adenocarcinoma cell lines, Gout et al. showed that SELE bound death receptor-3 on the cancer cells. Western blot analysis revealed that the SELE-binding protein was recognized by anti-DR3 antibodies. Anti-DR3 or knockdown of DR3 by small interfering RNA decreased adhesion of colon cancer cells to SELE and to SELE-expressing endothelial cells.
E-Selectin(SELE), also called Selectin E, ELAM1 or ELAM, is a cell adhesion molecule expressed only on endothelial cells activated by cytokines. It 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. E-Selection is a member of the selectin family of cell adhesion molecules. The E-Selectin gene is mapped on 1q24.2. The ELAM gene is present in single copy in the human genome and contains 14 exons spanning about 13 kb of DNA by Collins et al. Using affinity chromatography, pull-down assays, and mass spectrometric analysis on adenocarcinoma cell lines, Gout et al. showed that SELE bound death receptor-3 on the cancer cells. Western blot analysis revealed that the SELE-binding protein was recognized by anti-DR3 antibodies. Anti-DR3 or knockdown of DR3 by small interfering RNA decreased adhesion of colon cancer cells to SELE and to SELE-expressing endothelial cells.