Anti-CD62E antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CD62E also known as E-selectin or ELAM-1 is a cell adhesion molecule with a mass of approximately 115 kDa. It is present mainly on endothelial cells activated by cytokines. As a transmembrane glycoprotein E-selectin plays a mechanical role in mediating the tethering and rolling of leukocytes on the vascular endothelium during the inflammatory response. This function is important in directing leukocytes to sites of tissue damage or infection.

Biological function summary

E-selectin facilitates leukocyte adhesion by binding specific carbohydrate ligands on the surface of circulating immune cells. This binding is critical in the cascade of events that leads to leukocyte extravasation into tissues. E-selectin does not work in isolation rather forming part of a complex interaction with other cell adhesion molecules such as P-selectin and L-selectin. These interactions ensure precise control of cellular traffic during inflammatory responses.

Pathways

CD62E engages in the inflammatory signaling pathways including the NF-kB pathway. This pathway modulates the expression of E-selectin in response to pro-inflammatory cytokines like interleukin-1 and tumor necrosis factor-alpha. CD62E interacts with integrins on leukocytes and has downstream effects on cellular processes involved in immune response. Its cooperation with proteins like ICAM-1 and VCAM-1 further integrates it into a network of adhesion molecules maintaining vascular stability and immune surveillance.

Associated diseases and disorders

E-selectin expression is highly relevant in inflammatory diseases such as rheumatoid arthritis and atherosclerosis. These disorders involve chronic inflammation where the persistent activation of endothelial cells and overexpression of E-selectin contribute to pathology. The link with ICAM-1 in these settings suggests a mutual regulation between cell adhesion molecules enhancing leukocyte recruitment to inflamed tissues. This makes E-selectin not only a marker of endothelial activation but also a potential therapeutic target for modulating leukocyte adhesion in inflammatory diseases.