Related Experiment Videos
VE-cadherin: adhesion at arm's length.
Peter A Vincent1, Kanyan Xiao, Kathleen M Buckley
1Dept. of Dermatology, Emory Univ. School of Medicine, Woodruff Memorial Bldg., 1639 Pierce Drive, Atlanta, GA 30322, USA. akowalc@emory.edu
American Journal of Physiology. Cell Physiology
|April 13, 2004
Summary
Vascular endothelial cadherin (VE-cadherin) is crucial for blood vessel formation. Recent studies highlight p120-catenin
Area of Science:
- Cell Biology
- Molecular Biology
- Vascular Biology
Background:
- Vascular endothelial cadherin (VE-cadherin) is a key endothelial cell adhesion molecule.
- VE-cadherin plays critical roles in vascular permeability and remodeling.
- Catenins link cadherins to the cytoskeleton, mediating cell adhesion.
Purpose of the Study:
- To elucidate the role of catenins, particularly p120-catenin (p120(ctn)), in VE-cadherin function.
- To understand the regulatory mechanisms controlling VE-cadherin at the plasma membrane.
Main Methods:
- Structure-function analysis of the VE-cadherin extracellular domain.
- Identification and characterization of catenin binding partners.
- Investigation of p120(ctn) in mammalian cell membrane trafficking.
Main Results:
- p120-catenin (p120(ctn)) and related proteins are identified as crucial binding partners for VE-cadherin.
- p120(ctn) plays a significant role in regulating VE-cadherin membrane trafficking.
- A regulatory mechanism involving cadherin-catenin interactions controls cadherin levels at the plasma membrane.
Conclusions:
- p120-catenin (p120(ctn)) is central to a regulatory network governing VE-cadherin levels.
- This mechanism is vital for maintaining cadherin function in both epithelial and endothelial cells.
- Understanding this pathway is key for insights into vascular biology and cell adhesion.