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. 2017 Feb 22;7:43146. doi: 10.1038/srep43146

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Copyright © 2017, The Author(s)

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FAK can be activated in ischemic and hypoxic conditions; its downstream PI3K/AKT pathway is then activated through phosphorylation at the Tyr397 site, followed by mTOR/P70S6K activation. ERK1/2 can also be activated simultaneously. Both PI3K/AKT signalling and ERK1/2 are necessary for hypoxia-induced CF differentiation and ECM synthesis; this process also involves lysyl oxidase (LOX). Consequently, this response could be offset by FAK inhibitor.