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Rat VE-Cadherin / CD144 / CDH5 Protein (His Tag)

CDH5

Catalog Number P80276-R08H
Organism Species Rat
Host Human Cells
Synonyms CDH5
Molecular Weight The recombinant rat CDH5 comprises 572 amino acids and predicts a molecular mass of 65.1 kDa. The apparent molecular mass of the recombinant protein is approximately 91 kDa in SDS-PAGE under reducing conditions due to glycosylation.
predicted N Gly 25
SDS-PAGE
Purity > 70 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the rat CDH5 (NP_001100877.1) (Met1-Gln585) was expressed with a polyhistidine tag at the C-terminus.
Bio-activity
Research Area Cancer |Signal transduction |Cytoskeleton / ECM |Cell Adhesion |Cell Adhesion Molecules
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background Cadherins (Calcium dependent adhesion molecules) are a class of transmembrane proteins. Cadherin-5, also known as VE-cadherin, CDH5 and CD144, an endothelial specific cell-cell adhesion molecule, plays a pivotal role in the formation, maturation and remodeling of the vascular wall. VE-Cadherin is widely considered to be specific for vascular endothelia in which it is either the sole or the predominant cadherin, often co-existing with N-cadherin. This specificity of VE-cadherin for vascular endothelial cells is important not only in blood and lymph vessel biology and medicine, but also for cell-type-based diagnoses, notably those of metastatic tumors. As a classical cadherin, VE-Cadherin links endothelial cells together by homophilic interactions mediated by its extracellular part and associates intracellularly with the actin cytoskeleton via catenins. Mechanisms that regulate VE-cadherin-mediated adhesion are important for the control of vascular permeability and leukocyte extravasation. In addition to its adhesive functions, VE-Cadherin regulates various cellular processes such as cell proliferation and apoptosis and modulates vascular endothelial growth factor receptor functions. Consequently, VE-cadherin is essential during embryonic angiogenesis.
Reference
  • Taveau JC, et al. (2008) Structure of artificial and natural VE-cadherin-based adherens junctions. Biochem Soc Trans. 36(Pt 2): 189-93.
  • Vestweber D. (2008) VE-cadherin: the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation. Arterioscler Thromb Vasc Biol. 28(2): 223-32.
  • Gavard J. (2009) Breaking the VE-cadherin bonds. FEBS Lett. 583(1): 1-6.
  • Vestweber D, et al. (2009) Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player. Trends Cell Biol. 19(1): 8-15.
  • Boda-Heggemann J, et al. (2009) Beyond vessels: occurrence and regional clustering of vascular endothelial (VE-)cadherin-containing junctions in non-endothelial cells. Cell Tissue Res. 335(1): 49-65.