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. 2018 Jan 26;9(2):128. doi: 10.1038/s41419-017-0141-1

Fig. 4. SAA-iPSC exhibit deficient telomere elongation during reprogramming and telomere shortening upon hematopoietic differentiation.

Fig. 4

a Analysis of telomere length in parental fibroblasts (dark grey bars) and iPSC passage 30 (light blue bars) and 50 (green bars) in WT controls and SAA cell lines. One-way ANOVA with Tukey’s multiple comparison test was used for statistical comparison between fibroblasts and iPSC passage 30 and passage 50 (*p < 0.05); b Analysis of telomere length in iPSC passage 50 (green bars) and iPSC-based hematopoietic progenitors (HPC) differentiated from iPSC passage 50 (light grey bars) in WT controls and SAA cell lines. Multiple t-test using Holm-Sidak method was used for statistical comparison between iPSC passage 50 and HPC; c Analysis of telomerase activity in parental fibroblasts (dark grey bars) and iPSC at passage 30 (light blue bars) and 50 (green bars) in WT controls and SAA cell lines. One-way ANOVA with Tukey’s multiple comparison test was used for statistical comparison between fibroblasts and iPSC passage 30 and passage 50; d Analysis of telomerase activity in iPSC passage 50 (green bars) and iPSC-based hematopoietic progenitors (HPC) differentiated from iPSC passage 50 (light grey bars) in WT and SAA cell lines. Multiple t-test using Holm–Sidak method was used for statistical comparison between iPSC passage 50 and HPC. ad data is presented as mean of at least 3 independent experiments ± S.E.M. Data for all control cell lines is averaged in one group (WT)