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. 2015 Mar 11;5:8997. doi: 10.1038/srep08997

Figure 5. Haploid knockout of PIK3R1 activates WNT/β-catenin pathway dependent on the phosphorylation of AKT.

Figure 5

(a), The RT-PCR analysis of the mRNA expression of PIK3R1, CTNNB1, HES1, GLI1, and NANOG in 786-O, 786-mut1, 786-mut2, A-704, A-704-mut1, and A-704-mut2 cells. (b), 786-O, 786-mut1, 786-mut2, A-704, A-704-mut1, and A-704-mut2 cell lysates were immunoprecipitated by anti-PIK3R1 antibody and immunoblotted with anti-PIK3R1 (upper panel) and anti-P110 antibody (middle panel). Whole lysates immunobotted with anti-P110 antibody (lower panel) served as control. (c), The WB analysis of p-AKT and p-ERK in 786-O, 786-mut1, 786-mut2, A-704, A-704-mut1, and A-704-mut2 cells. AKT and ERK served as control. (d), The WB analysis of CTNNB1, p-GSK3β, GSK3β in 786-O, 786-mut1, 786-mut2, A-704, A-704-mut1, and A-704-mut2 cells. (e), The WB analysis of AKT, pAKT, pGSK3β, GSK3β, and CTNNB1 in 786-mut1 shCtrl, 786-mut1 shAKT, A-704-mut2 sh Ctrl, and A-704-mut2 shAKT cells. The RT-PCR analysis of AKT in 786-mut1 shCtrl, 786-mut1 shAKT, A-704-mut2 shCtrl, and A-704-mut2 shAKT cells. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01.