Neonatal maternal separation (MS) lead to increased anxiety-like behavior in Cdh13(-/-) mice compared to the other two MS groups. Cdh13(-/-) mice showed a context-dependent effect on stress- & anxiety-related behavior impaired extinction learning following contextual fear conditioning & decreased impulsivity & a mild decrease in errors in the Barnes maze & reduced risk-taking in the light-dark transition test after MS.
Findings show that Cdh13 is critical for inhibitory function of Golgi cells and that GlyT2::Cre-mediated deletion of Cdh13 in non-executive centers of the brain such as the cerebellum may contribute to cognitive and social behavioral deficits linked to neurological disorders.
using rat and murine aortic smooth muscle cells as experimental models we surveyed the ability of T-cadherin to regulate autophagy in SMCs during serum-starvation stress. Overall our findings have identified T-cadherin as a novel positive regulator of autophagy and survival in smooth muscle cells
a unique key feature of the T-cad prodomain is its involvement in binding of the T-cad repeats 1 and 2 to adiponectin; adiponectin positively regulates T-cad abundance
T-cadherin was essential for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions and the adiponectin-T-cadherin association protected against vascular injury.
CDH13 is a negative regulator of inhibitory synapses in the hippocampus and provide insights into how CDH13 dysfunction may contribute to the excitatory/inhibitory imbalance observed in Attention Deficit Disorder with Hyperactivity.
These data show that both circulating and tissue-bound Adipo levels are dependent on Tcad and in reverse regulate tissue Tcad levels through a positive feedback loop.
These data highlight a previously unrecognized role for T-cadherin in limb revascularization and show that it is essential for mediating the vascular actions of adiponectin.
T-cadherin is a component of insulin granules suggesting that it contributes to the regulation of insulin secretion independently of direct interactions with adiponectin.
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