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. 2020 Jan 28;11(1):71. doi: 10.1038/s41419-020-2265-y

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© The Author(s) 2020

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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Fig. 2 — a Confirmation of some results from RNA-seq by RT-qPCR in different cells. Log₂ mRNA levels of TNFAIP3, IκBα, and NF-κB1 in PARP1-KO or complemented cells were normalized to that in corresponding parental cells. Error bars represent the SD. b Confirmation of some results from RNA-seq by western blotting in indicated cells. c Loss of PARP1 increased mRNA and protein levels of FoxO1, which was prevented, at least partially, by PARP1 complementation. The mRNA levels of FoxO1 were detected by RT-qPCR and normalized to that in the corresponding parental cells; Error bars represent the SD. *, p < 0.05. Protein levels of FoxO1 were detected by western blotting. d After RD-ES cells were transfected with GFP-PARP1 cDNA for 72 h, protein levels of FoxO1 were determined by western blotting. The relative FoxO1 levels were presented as the ratio of (FoxO1/GAPDH)_GFP-PARP1/(FoxO1/GAPDH)_CON when the value of (FoxO1/GAPDH)_CON was normalized as 1.