Research & Publications
We are interested in the control of vascular remodeling. Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is up-regulated in the neointima of remodeling arteries and modulates vascular smooth muscle cell (VSMC) growth. Receptor tyrosine kinases (RTKs) constitute a family of cell-surface receptors, including PDGFR, EGFR, VEGFR, and FGFR, controlling a variety of cellular processes, such as proliferation, differentiation, migration, and survival. RTKs are activated by binding of extracellular ligands, resulting in increased tyrosine kinase activity and phosphorylation of target proteins. Once activated, RTKs are ubiquitinated, internalized and targeted for degradation to the lysosomal compartment or locally destroyed in proteasomes. Many of these processes are regulated by ubiquitination, a post-traslational modifi cation where the small protein ubiquitin is covalently attached to a target protein by ubiquitin ligases such as c-Cbl. While polyubiquitination marks proteins for proteasomal degradation, mono- or multi-ubiquitination is sufficient to direct endocytosis and lysosomal degradation of membrane receptors.
Specialized Terms: vascular remodeling, receptor tyrosine kinases (RTKs)
Extensive Research Description
Continued detailed analyses of the involvement of ESDN in the regulation of RTK-driven pathologies is thus predicted to pave the way for therapeutic strategy for vascular diseases and other diseases involving RTK-driven tissue remodeling.
Nephrology; Vascular Remodeling