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α~5~β~1~ integrin stimulates Bcl‐2 expression and cell survival through Akt, focal adhesion kinase, and Ca^2+^/calmodulin‐dependent protein kinase IV by Byung‐Heon Lee; Erkki Ruoslahti is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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CHO cells expressing a 5 b 1 integrin are more resistant to apoptosis and express more Bcl-2 than the same cells engineered to express a v b 1 or cytoplasmically truncated a 5 Dcb 1 integrin as their main fibronectin receptor. The Bcl-2 up-regulation by a 5 b 1 is mediated, at least in part, by the focal adhesion kinase (FAK) and phosphatidylinositol-3 kinase (PI3K)/Akt pathways. Here, we show that integrin-mediated activation of Ca 2þ /calmodulin-dependent protein kinase (CaMK) IV, and the NF-kB and CREB transcription factors also enhance the integrin-dependent regulation of Bcl-2 expression in the a 5 b 1 cells. A forkhead transcription factor, which is inactivated by Akt, blocked Bcl-2 expression. The FAK pathway was found to be defective in both the a v b 1 and a 5 Dcb 1 cells. These cell lines differed from one another in two Bcl-2-regulating pathways: adhesion through a v b 1 failed to activate Akt, allowing forkhead to suppress Bcl-2 transcription, whereas a 5 Dcb 1 did not activate NF-kB and CREB, presumably because CaMK IV was not activated. Our results indicate that three pathways, the FAK, PI3K/Akt, and CaMK IV mediate the survival-supporting activity of a 5 b 1 integrin

Who reads α~5~β~1~ integrin stimulates Bcl‐2 expression and cell survival through Akt, focal adhesion kinase, and Ca^2+^/calmodulin‐dependent protein kinase IV?

Author

Byung‐Heon Lee; Erkki Ruoslahti

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2005

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)