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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. 6 — Bim expression is responsible for the defective thymocyte development in NCoR1-deficient mice. a Flow cytometry analysis of CD4 and CD8 expression on thymocytes from wild-type (WT), NCoR1-deficient (cKO), Bim KO, Ncor1 and Bim double-knockout (dKO) mice. b The number of cells in each subpopulation gated in (a). c Expression of CD62L vs. CD69 or CD24 on CD4⁺ single-positive (SP) thymocytes from WT, cKO, Bim KO, and dKO mice. d The percentages of CD69- and CD5-positive subpopulations in (c). e Flow cytometry analysis of CD69 and CD5 expression on total thymocytes from WT, cKO, Bim KO, and dKO mice. f Intracellular levels of the active caspase-3 (Act.Casp.3) in thymocytes activated in vitro for 1 h. The data are representative of two independent experiments (n = 2 or 3). Statistical significance was analyzed using the two-tailed Student’s t test (*P < 0.05; **P < 0.01; ***P < 0.001; NS, not significant)