Endothelial cell surface expressed chemotaxis and apoptosis regulator (ECSCR)

Endothelial cell surface expressed chemotaxis and apoptosis regulator (ECSCR) is a single-pass transmembrane glycoprotein primarily expressed in endothelial cells and, to a lesser extent, in white adipocytes[1][2]. ECSCR modulates endothelial migration, chemotaxis, tube formation, and plays a critical role in angiogenesis by interacting with key molecular partners including vascular endothelial growth factor receptor 2 (VEGFR-2) and PTEN[1][2]. By influencing these pathways, ECSCR regulates vascular homeostasis, contributes to the control of lipolysis in adipose tissue, and is implicated in metabolic processes such as insulin signaling and energy metabolism[1][2]. Loss of ECSCR results in impaired insulin signaling, elevated triglycerides, and disrupted lipid metabolism, suggesting its importance for metabolic health[1]. ECSCR is also enriched in tumor and inflammatory vascular contexts and is considered a promising target in diseases such as cancer, cardiovascular disease, and metabolic syndrome[2]. Alternative splicing produces multiple isoforms that modulate various cell behaviors[2]. No direct drug interactions, biomarkers, or safety challenges specific to ECSCR have been reported in the references provided.

Other names

Endothelial cell-specific chemotaxis regulatorECSM2ARIAEndothelial cell-specific molecule 2Apoptosis regulator through modulating IAP expression

No specific drug mechanisms reported; ECSCR is mechanistically involved in VEGFR-2 signaling, PTEN-AKT pathway, and insulin response