Model showing how AMPK loss promotes tensin-mediated integrin activity. In the absence of AMPK, the transcriptional constraints that limit tensin expression are removed. A corresponding increase in tensin expression leads to enhanced tensin binding to β1-integrin tails to support integrin activity after initial integrin activation by talin. This leads to enhanced fibrillar adhesion formation and integrin-dependent processes such as mechanotransduction and fibronectin remodeling. P, phosphorylated.