JAM-A regulates epithelial proliferation through Akt/β-catenin signalling
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Updated: Jun 3, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Porfirio Nava1, Christopher T Capaldo, Stefan Koch
1Epithelial Pathobiology Research Unit, Department of Pathology, Emory University, Whitehead Biomedical Research Building, Room 105E, 615 Michael Street, Atlanta, Georgia 30322, USA.
Abstract:
Expression of the tight junction protein junctional adhesion molecule-A (JAM-A) has been linked to proliferation and tumour progression. However, a direct role for JAM-A in regulating proliferative processes has not been shown. By using complementary in vivo and in vitro approaches, we demonstrate that JAM-A restricts intestinal epithelial cell (IEC) proliferation in a dimerization-dependent manner, by inhibiting Akt-dependent β-catenin activation. Furthermore, IECs from transgenic JAM-A(-/-)/β-catenin/T-cell factor reporter mice showed enhanced β-catenin-dependent transcription. Finally, inhibition of Akt reversed colonic crypt hyperproliferation in JAM-A-deficient mice. These data establish a new link between JAM-A and IEC homeostasis.
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