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. 2017 Oct 16;8:959. doi: 10.1038/s41467-017-00931-8

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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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Fig. 3 — Deletion of NCoR1 causes elevated thymocyte apoptosis. a Flow cytometry analysis of CD69 expression on sorted in vitro-stimulated CD4⁺CD8⁺ double-positive (DP) thymocytes from NCoR1-deficient (cKO) and wild-type (WT) mice (n = 3). b The mean fluorescence intensity of CD69 expression in (a). c Intracellular levels of the active caspase-3 (Act.Casp.3) detected by flow cytometry in cKO and WT thymocytes after in vitro TCR stimulation for indicated amounts of time (n = 3 for each group). d, e Intracellular levels of the active caspase-3 (Act.Casp.3) detected by flow cytometry in freshly isolated thymocytes (n = 4 to 5). f TUNEL staining of the thymus sections of cKO and WT mice (n = 10). The scale bars indicate 100 μm. g Quantification of the apoptotic cells in (f). The data are representative of two independent experiments (a–e). Statistical significance was analyzed using the two-tailed Student’s t test (*P < 0.05; **P < 0.01; ***P < 0.001)