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. 2017 Oct 13;3(4):358–365. doi: 10.1007/s40778-017-0100-x

Fig. 1.

Fig. 1

Diagram illustrating FAK signaling in hESCs. Stable ECM/integrin interaction induces activation of FAK, phosphorylated at Y397, at the cell surface, initiating the transduction of attachment cues to the cell. In turn, FAK Y397 activates the PI3K survival cascade, leading to phosphorylation of AKT and its downstream target MDM2. This allows MDM2 to continuously ubiquitinate p53 targeting it for proteosome degradation and maintaining low levels so that it cannot induce differentiation or apoptosis. In addition, FAK is localized in the nucleus where it binds pluripotency factors but can also exert its scaffolding roles in support of MDM2