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Biochemistry (Mosc). 2009 Apr;74(4):362-70.

T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability.

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1
Institute of Experimental Cardiology, Cardiology Research Center, Moscow, 121552, Russia.

Abstract

In the present study, expression of T-cadherin was shown to induce intracellular signaling in NIH3T3 fibroblasts: it activated Rac1 and Cdc42 (p < 0.01) but not RhoA. T-Cadherin overexpression in human umbilical vein endothelial cells (HUVEC) using adenoviral constructs induced disassembly of microtubules and polymerization of actin stress fibers, whereas down-regulation of endogenous T-cadherin expression in HUVEC using lentiviral constructs resulted in microtubule polymerization and a decrease in the number of actin stress fibers. Moreover, suppression of the T-cadherin expression significantly decreased the endothelial monolayer permeability as compared to the control (p < 0.001).

PMID:
19463088
[Indexed for MEDLINE]
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