Figure 3.
Telomere length and proliferative capacity can be restored by hemizygous disruption of TINF2 in hESCs. (A) Schematic overview: CAS9-mediated double-strand break in exon 2 to disrupt the disease allele of TINF2. (B) Relative expression level of TIN2 in the WT/null cells relative to the heterozygous (het) mutant hESCs (WT/T284R) normalized to GAPDH. Error bars indicate the SD, n = 3. (C) Western blot analysis of the het (WT/T284R) and het WT/c.568insT (WT/null) hESCs. (D) Telomere length analysis of the WT/T284R and WT/null hESCs. Each time point sample was collected weekly over 3 consecutive weeks. (E) Growth curves of cumulative PDs over days after differentiation for WT, WT/T284R, and WT/null cells.

Telomere length and proliferative capacity can be restored by hemizygous disruption of TINF2 in hESCs. (A) Schematic overview: CAS9-mediated double-strand break in exon 2 to disrupt the disease allele of TINF2. (B) Relative expression level of TIN2 in the WT/null cells relative to the heterozygous (het) mutant hESCs (WT/T284R) normalized to GAPDH. Error bars indicate the SD, n = 3. (C) Western blot analysis of the het (WT/T284R) and het WT/c.568insT (WT/null) hESCs. (D) Telomere length analysis of the WT/T284R and WT/null hESCs. Each time point sample was collected weekly over 3 consecutive weeks. (E) Growth curves of cumulative PDs over days after differentiation for WT, WT/T284R, and WT/null cells.

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