Figure 2
Figure 2. Transgene correction of GT iPSC lines. (A) Quantitative reverse transcriptase polymerase chain reaction analysis of expression of the Gp1ba promoter construct, endogenous ITGA2B, and endogenous ITGB3 in control, uncorrected GT, and corrected GT iPSC-derived megakaryocytes relative to cyclophilin (mean ± SEM for 3 replicates). (B) Analysis by flow cytometry of CD41 vs CD42 expression in control, GT, and corrected GT iPSC lines differentiated into megakaryocytes. (C) Bar graphs of gated populations in Figure 2B (gray rectangles) examine expression of CD41 of corrected GTP1 and GTP2 relative to two different control iPSC-derived megakaryocytes (mean ± SEM for 3 independent experiments). (D) PAC-1 and fibrinogen binding in convulxin-stimulated uncorrected and corrected GT megakaryocytes relative to control megakaryocytes (mean ± SEM for 3 independent experiments).

Transgene correction of GT iPSC lines. (A) Quantitative reverse transcriptase polymerase chain reaction analysis of expression of the Gp1ba promoter construct, endogenous ITGA2B, and endogenous ITGB3 in control, uncorrected GT, and corrected GT iPSC-derived megakaryocytes relative to cyclophilin (mean ± SEM for 3 replicates). (B) Analysis by flow cytometry of CD41 vs CD42 expression in control, GT, and corrected GT iPSC lines differentiated into megakaryocytes. (C) Bar graphs of gated populations in Figure 2B (gray rectangles) examine expression of CD41 of corrected GTP1 and GTP2 relative to two different control iPSC-derived megakaryocytes (mean ± SEM for 3 independent experiments). (D) PAC-1 and fibrinogen binding in convulxin-stimulated uncorrected and corrected GT megakaryocytes relative to control megakaryocytes (mean ± SEM for 3 independent experiments).

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