Fig. 2: ZNF768 depletion increases p53 levels and causes premature senescence in MEFs.
From: ZNF768 loss amplifies p53 action and reduces lung tumorigenesis in mice
A Western blot showing the expression of ZNF768 and p53 in ZNF768 wild-type and knockout MEFs at P4. B-ACTIN was used as a loading control. Representative samples are shown. B Quantification of p53 protein levels from the Western blot described in (A) (n = 5-8 cell lines/group). Data represent the mean ± SEM. Significance was determined by 2-tailed, unpaired t-test. *P < 0.05 versus controls. C ZNF768 wild-type and knockout MEFs were treated with doxorubicin for 24 h (0 to250 nM). The cells were next washed and followed for 48 h and RNA was harvested. The expression of indicated genes was measured by RT-qPCR (n = 5 cell lines/group). Data represent the mean ± SEM. Significance was determined by 2-way ANOVA. *P < 0.05, **P < 0.01 ***P < 0.001 versus controls. D ZNF768 wild-type and knockout MEFs were treated as described in (C) and counted starting at doxorubicin treatment (n = 5-8 cell lines/group). Data represent the mean ± SEM. Significance was determined by 2-way ANOVA. ***P < 0.001 versus controls. E Growth curve of ZNF768 wild-type and knockout MEFs cultured under the standard 3T3 protocol (n = 4 cell lines/group). Data represent the mean ± SEM. Significance was determined by 2-way ANOVA. ***P < 0.001 versus controls. This experiment was reproduced twice in distinct cell lines. F Western blot showing the expression of ZNF768, total and phosphorylated p53, and p21 in ZNF768 wild-type and knockout MEFs at P7. B-ACTIN was used as a loading control. Representative samples are shown.
