Recombinant Human E-selectin

Background

Selectin E (SELE) is an adhesion molecule expressed on activated endothelial cells in response to inflammatory cytokines such as TNF-α and IL-1β, playing a pivotal role in the recruitment of leukocytes to sites of inflammation. It mediates the rolling and tethering of leukocytes on the endothelium by binding to specific glycoprotein ligands on the surface of leukocytes, such as PSGL-1, facilitating their migration into tissues. SELE is crucial in early-stage inflammatory responses and is involved in various pathophysiological processes, including atherosclerosis, autoimmune diseases, and cancer metastasis. Dysregulation of SELE expression has been associated with increased endothelial dysfunction and vascular inflammation, contributing to the development of cardiovascular diseases. Its expression is transient and tightly regulated by transcriptional mechanisms, ensuring that leukocyte recruitment occurs precisely during inflammatory responses. Therapeutic targeting of SELE has been explored to mitigate excessive inflammation, with strategies focusing on blocking its interaction with ligands to prevent leukocyte adhesion and infiltration. Additionally, SELE is being investigated as a biomarker for endothelial activation and vascular inflammation in conditions such as sepsis and chronic inflammatory disorders. Its role in mediating cell adhesion under shear stress highlights its importance in maintaining vascular integrity during immune surveillance and inflammatory responses.