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. 2020 Jul 31;31(2):187–205. doi: 10.1038/s41422-020-0385-7

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© Center for Excellence in Molecular Cell Science, CAS 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. 5 — a Top, schematic diagram showing the mutation strategy for CLOCK. Bottom, Co-IP of KAP1 and nuclear lamina proteins with exogenous WT and mutant CLOCK proteins (Mut A and Mut B) in HEK293T cells. Data are representative of two independent experiments. The red asterisk indicates the LBR band pulled down by IP with Flag antibody. b SA-β-gal staining in CLOCK^–/– hMSCs transduced with lentiviruses expressing Luc, CLOCK (WT), CLOCK (Mut A), or CLOCK (Mut B). The percentage of SA-β-gal-positive cells in each cell type was normalized to that in CLOCK^−/− hMSCs transduced with Luc. Data are presented as means ± SEM. n = 3 biological replicates. ***P < 0.001 (two-tailed unpaired Student’s t-test). Scale bars, 100 μm. c Clonal expansion assay of CLOCK^−/− hMSCs transduced with lentiviruses expressing Luc, CLOCK (WT), CLOCK (Mut A), or CLOCK (Mut B). The clonal expansion ability of each cell type was normalized to that of CLOCK^–/– hMSCs transduced with Luc. Data are presented as means ± SEM. n = 3 biological replicates. **P < 0.01 (two-tailed unpaired Student’s t-test). d Top, schematic diagram showing the mutation strategy for the CLOCK Δ51 truncation. Bottom, relative mRNA levels of PER3 and NR1D2 in CLOCK^+/+ hMSCs and CLOCK^−/− hMSCs transduced with lentiviruses expressing Luc, CLOCK (WT), or CLOCK (Δ51). Data are presented as means ± SEM. n = 4. ***P < 0.001 (two-tailed unpaired Student’s t-test). Data are representative of two independent experiments. e Co-IP of KAP1 and nuclear lamina proteins with exogenous CLOCK (WT) and CLOCK (Δ51) proteins in HEK293T cells. Data are representative of two independent experiments. The red asterisk indicates the band of Lamin B1. f SA-β-gal staining of CLOCK^−/− hMSCs transduced with lentiviruses expressing Luc, CLOCK (WT), or CLOCK (Δ51). The percentage of SA-β-gal-positive cells in each cell type was normalized to that in CLOCK^–/– hMSCs transduced with Luc. Data are presented as means ± SEM. n = 3 biological replicates. **P < 0.01 (two-tailed unpaired Student’s t-test). Scale bars, 100 μm. g Clonal expansion assay of CLOCK^–/– hMSCs transduced with lentiviruses expressing Luc, CLOCK (WT) and CLOCK (Δ51). The clonal expansion ability of each cell type was normalized to that of CLOCK^–/– hMSCs transduced with Luc. Data are presented as means ± SEM. n = 3 biological replicates. ***P < 0.001 (two-tailed unpaired Student’s t-test).