PMC:3583298 / 22202-23136 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/3583298","sourcedb":"PMC","sourceid":"3583298","source_url":"https://www.ncbi.nlm.nih.gov/pmc/3583298","text":"To address whether IGF2/Akt activity regulates the YAP-associated DNA damage response defect after radiation, we used Shh-treated CGNP cultures. Confirming our observations (Figure 5), YAP infection is associated with increased Akt activity (Figure 6A) as determined by phosphorylation of S473. Treatment of YAP-infected CGNPs with the drug LY294002, which inhibits phosphoinositide-3 kinase, the upstream activator of Akt, reduced levels of S473-phosphorylated Akt. After irradiation, we saw induction of ATM phosphorylation in GFP- and YAP-infected CGNPs, although to a lesser extent in the presence of ectopic YAP, indicating reduced activity of this kinase. In keeping with reduced ATM activity in the presence of YAP, we also observed reduced Chk2 phosphorylation. In the presence of LY294002, full ATM and Chk2 phosphorylation were recovered, indicating that YAP requires Akt activity for its suppressive effect on ATM and Chk2.","tracks":[]}