T-cadherin [SEP] found in taxon
lipoproteins (LDL) in vascular smooth muscles (VSMCs), T-cadherin was isolated and identified as new LDL receptor using human aortic media and the ligand-blotting method. The properties of T-cadherin as an LDL receptor were markedly different from the presently known types of LDL receptors. LDL binding to T-cadherin leads to the activation of Erk 1/2 tyrosine kinase and the nuclear translocation of NF-kappaB.
T-cadherin overexpression in ECs facilitates spontaneous cell migration, formation of stress fibers and change of the phenotype
PDGF)-BB, epidermal growth factor (EGF) or insulin-like growth factor (IGF) elicit a reversible dose- and time-dependent decrease in T-cadherin expression in cultured VSMCs.
Expression of T-cadherin leads to complete inhibition of subcutaneous tumor growth in nude mice. Seeding T-cadherin expressing cells on plastic coated with recombinant aminoterminal fragments of T-cadherin resulted in suppression of cell growth and was found to be associated with increased expression of p21. In T-cadherin deficient C6 glioma cell lines, its overexpression