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. 2017 Sep 6;7:10739. doi: 10.1038/s41598-017-11208-x

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Regulation of CD137L, CDC42BPG and FST by p53. (a) Outline of the screening process. The expression profiles of 23813 genes in calvarial bone were detected by RNA sequencing, and 69 genes were selected by the indicated criteria as p53-induced genes. A second screening revealed three novel direct p53 targets. Of the 3 genes, one gene (CD137L) was up-regulated specifically in bone among 24 tissues. (b) At 24 h after transfection of each siRNA, U2OS cells were treated with ADR (2 μg/ml for 2 h). At 36 h after treatment, qPCR was performed. siRNA against EGFP was used as a control. β-actin was used for the normalization of expression levels. Error bars represent SD (n = 2). (c) qPCR was performed for the same calvaria sample as the RNA sequencing. β-actin was used for normalization of the expression levels. Error bars represent SD (n = 3). **P < 0.001, Student’s t-test. (d) qPCR was performed 36 h after treatment with ADR (2 μg/ml for 2 h) in p53 ^+/+ or p53 ^−/− calvarial osteoblasts. β-actin was used for normalization of the expression levels. Error bars represent SD (n = 3). **P < 0.001, Student’s t-test.