The identification of specific signaling partners and understanding the pathways influenced by T-cadherin are active areas of research, highlighting its potential role in vascular biology and disease pathologies.

T-cadherin overexpression in ECs facilitates spontaneous cell migration, formation of stress fibers and change of the phenotype from quiescent to promigratory.

T-cadherin is highly expressed in the heart, aortic wall, neurons of the brain cortex and spinal cord and also in the small blood vessels in spleen and other organs.

T-cadherin expression in arterial wall after balloon angioplasty correlates with late stages of neointima formation and coincidentally with the peak in proliferation and differentiation of vascular cells.

It is highly expressed in adventitial vasa vasorum of injured arteries suggesting the involvement of T-cadherin in the processes of angiogenesis after vessel injury.

Adiponectin (adipocyte complement-related protein of 30 kDa) is a cytokine produced by adipose tissue and its deficiency is associated with metabolic syndrome, obesity, type II diabetes and atherosclerosis.

In cultured VSMC and primary astrocytes, the expression of T-cadherin depends on proliferation status with maximum at confluency suggesting its regulation of cell growth by contact inhibition.

In T-cadherin deficient C6 glioma cell lines, its overexpression results in growth suppression involving p21Cip1/WAF1 production and G2 arrest.

Furthermore, T-cadherin overexpression was found to be a common feature of human high grade astrocytomas and associated with malignant transformation of astrocytes.

Hetezygosity for NF1 (neurofibromatosis 1) tumor suppressor resulting in reduced attachment and spreading and increased motility also coincides with upregulated T-cadherin expression.

Data show that HUVEC cells overexpressing T-cadherin after adenovirus infection enter S-phase more rapidly and exhibit increased proliferation potential.

T-cadherin was originally cloned from chick embryo brain, where it was implicated as a negative guiding cue for motor axon projecting through the somitic sclerotome and presumably for migrating neural crest cells .