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Publication : Focal adhesion kinase is required for β-catenin-induced mobilization of epidermal stem cells.

First Author  Ridgway RA Year  2012
Journal  Carcinogenesis Volume  33
Issue  12 Pages  2369-76
PubMed ID  22971575 Mgi Jnum  J:193298
Mgi Id  MGI:5468088 Doi  10.1093/carcin/bgs284
Citation  Ridgway RA, et al. (2012) Focal adhesion kinase is required for beta-catenin-induced mobilization of epidermal stem cells. Carcinogenesis 33(12):2369-76
abstractText  Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that integrates signals downstream of integrin and growth factor activation. Previously, we have shown that skin-specific loss of fak prevents chemically induced skin carcinogenesis in mice following phorbol ester treatment. In this study, we show that skin-specific deletion of fak prevents mobilization of stem cells within the bulge region of the hair follicle, which are the precursors of papillomas following phorbol ester treatment. We also show that phorbol ester treatment results in activation of-catenin within the skin and that FAK is required for beta-catenin-induced stem cell mobilization. In addition, inhibition of Src kinase activity, a major binding partner of FAK also prevents stem cell mobilization. We show that FAK is required for the nuclear localization of beta-catenin in the skin following phorbol ester treatment and the transcriptional activation of the beta-catenin target gene c-Myc. This provides the first evidence of cross-talk between integrin and Wnt signalling pathways in the control of epidermal stem cells and the early events associated with skin carcinogenesis.
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