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. 2017 Mar 10;312(5):L722–L730. doi: 10.1152/ajplung.00478.2016

Fig. 5.

Fig. 5.

Active FAK inhibits caspase-8-mediated activation of apoptosis. A: caspase-8 activation by primary AECs from SC FAK or littermate control mice in response to transforming growth factor-β (TGF-β); n = 5. P < 0.05, compared with control AECs treated with TGF-β. B: caspase-8 activation by primary AECs from wild-type mice in response to TGF-β and treated with PF-573228 (FAK Inh) or vehicle control; n = 5. *P < 0.05, compared with AECs treated with DMSO control and TGF-β. C: caspase-3/7 activation by wild-type primary AECs in response to TGF-β and treated with PF-573228 (FAK Inh) or vehicle control and Z-IETD-FMK (Casp8 Inh) or vehicle control; n = 5. *P < 0.05, compared with AEC treated with TGF-β and FAK inhibitor without Casp8 Inh. D: immunoprecipitation (IP) for FAK from wild-type or FAK-null primary AEC lysate treated with PF573228 or vehicle control and immunoblotted for Casp8, FAK, and phospho-FAK (p-FAK). Immunoblot of 5% of lysate used for immunoprecipitation (lysate) is also shown. E: immunoprecipitation for Casp8 from wild-type or FAK-null primary AEC lysate treated with PF573228 or vehicle control and immunoblotted for Casp8, FAK, and p-FAK. Immunoblot of 5% of lysate used for immunoprecipitation (lysate) is also shown.