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Papers In Press, published online ahead of print July 21, 2005
Department of Epithelial Stem Cell Research Center, Veneto Eye Bank Foundation, Venezia 30122
Corresponding Author: enzo.calautti{at}cbrc2.mgh.harvard.edu
Signaling pathways regulating the differentiation program of epidermal cells widely overlap with those activated during apoptosis. How differentiating cells remain protected from premature death, however, is still poorly defined. We show here that the PI3K/Akt pathway is activated at early stages of mouse keratinocyte differentiation both in culture and in the intact epidermis in vivo. Expression of active Akt in keratinocytes promotes growth arrest and differentiation, whereas pharmacological blockade of PI3K inhibits the expression of ‘late’ differentiation markers and leads to death of cells that would otherwise differentiate. Mechanistically, the activation of the PI3K/Akt pathway in keratinocyte differentiation depends on the activity of the EGFR and Src family of tyrosine kinases and the engagement of E-cadherin mediated adhesion. During this process, PI3K increasingly associates with cadherin-catenin protein complexes bearing tyrosine phosphorylated YxxM motifs. Thus, the PI3K signaling pathway regulates the choice between epidermal cell differentiation and death, at the cross-talk between tyrosine kinases and cadherin-associated catenins.
J. Biol. Chem, 10.1074/jbc.M506119200
Submitted on June 6, 2005
Revised on July 15, 2005
Accepted on July 21, 2005
Phosphoinositide 3-kinase signaling to AKT promotes keratinocyte differentiation versus death
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