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Publication : Focal adhesion kinase/Src suppresses early chondrogenesis: central role of CCN2.

First Author  Pala D Year  2008
Journal  J Biol Chem Volume  283
Issue  14 Pages  9239-47
PubMed ID  18276598 Mgi Jnum  J:135567
Mgi Id  MGI:3794128 Doi  10.1074/jbc.M705175200
Citation  Pala D, et al. (2008) Focal adhesion kinase/Src suppresses early chondrogenesis: central role of CCN2. J Biol Chem 283(14):9239-47
abstractText  Adhesive signaling plays a key role in cellular differentiation, including in chondrogenesis. Herein, we probe the contribution to early chondrogenesis of two key modulators of adhesion, namely focal adhesion kinase (FAK)/Src and CCN2 (connective tissue growth factor, CTGF). We use the micromass model of chondrogenesis to show that FAK/Src signaling, which mediates cell/matrix attachment, suppresses early chondrogenesis, including the induction of Ccn2, Agc, and Sox6. The FAK/Src inhibitor PP2 elevates Ccn2, Agc, and Sox6 expression in wild-type mesenchymal cells in micromass culture, but not in cells lacking CCN2. Our results suggest a reduction in FAK/Src signaling is a critical feature permitting chondrogenic differentiation and that CCN2 operates downstream of this loss to promote chondrogenesis.
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