Disease relevance of Cdh13

• We further demonstrate that transient and stable reexpression of T-cadherin in deficient C6 glioma cell lines results in growth suppression [1].
• Based on recent studies from our laboratory implicating T-cadherin expression in mouse brain tumorigenesis, we examined the role of T-cadherin in astrocytoma growth regulation [1].

High impact information on Cdh13

• T-cadherin-expressing C6 cell lines exhibited increased p21(CIP1/WAF1), but not p27(Kip1), expression [1].
• T-cadherin-mediated cell growth regulation involves G2 phase arrest and requires p21(CIP1/WAF1) expression [1].
• Cell cycle flow cytometry demonstrated that T-cadherin reexpression resulted in G2 phase arrest, which was confirmed by mitotic index analysis [1].
• In addition, T-cadherin-expressing C6 cell lines demonstrated increased homophilic cell aggregation, increased cell attachment to fibronectin, and decreased cell motility [1].
• In this report, we show that T-cadherin expression increased during primary astrocyte physiologic growth arrest in response to contact inhibition and serum starvation in vitro, suggesting a function for T-cadherin in astrocyte growth regulation [1].

Biological context of Cdh13

• Together the data support an association between T-cadherin expression and SMC phenotype [2].
• Staining for monocyte/macrophage antigen ED-1, proliferating cell nuclear antigen and smooth muscle alpha-actin revealed that spatial and temporal changes in T-cadherin level coincided with the peak in cell migration and proliferation activity during neointima formation [2].
• We have cloned rat T-cadherin cDNA encoding the full length amino acid sequence [3].
• The 5(') untranslated nucleotide sequences of rat, mouse, and human T-cadherin contain a conserved GCGTG motif which constitutes the invariant core sequence of dioxin- or xenobiotic-regulatory elements [3].
• CONCLUSION: In vascular cells, T-cad is dynamically regulated during the cell cycle and its expression functions in the promotion of proliferation [4].

Anatomical context of Cdh13

• Lastly, T-cadherin-mediated growth arrest was dependent on p21(CIP1/WAF1) expression and was eliminated in p21(CIP1/WAF1)-deficient fibroblasts [1].
• Here we performed immunohistochemical analysis of spatial and temporal changes in vascular T-cadherin expression following balloon catheterisation of the rat carotid artery [2].
• Aryl hydrocarbon receptor ligands repress T-cadherin expression in vascular smooth muscle cells [3].
• Using cultures of rat aortic smooth muscle cells this study presents data revealing T-cadherin as a putative target gene for negative regulation of expression through AHR signalling [3].

Other interactions of Cdh13

• T-cadherin is a glycosyl phosphatidylinositol-anchored member of the cadherin superfamily of adhesion molecules [2].

References