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. 2015 Sep 17;44(1):164–174. doi: 10.1093/nar/gkv927

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Repression of non-canonical CHR-containing genes by p53 requires p21 and is conserved between mouse and human. The log₂-fold change of mRNA expression from treated compared to untreated (A) NIH3T3, (B) HCT116 wild-type, (C) HCT116 p21^−/− and (D) HFF cells is displayed. Cells were treated with doxorubicin, nutlin-3a or 5-FU for 24 h. Untreated cells and cells treated with DMSO served as controls. Normalization was carried out against measurements from untreated cells. GAPDH, L7 and U6 served as negative controls for p53 response, while CDKN1A and MDM2 were employed as positive controls. (A–C) Experiments were performed with two biological replicates and three technical replicates each (n = 6). (D) Experiments were performed with three technical replicates (n = 3). Significance of changes in expression levels was tested against GAPDH expression levels using the unpaired Student's t-test; n.s. not significant; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001.