Abstract
Genetic mutations in TP53 contribute to multiple human cancers. Here we report the generation of a H1-p53(R248W/R248W) human embryonic stem cell line harboring a homozygous TP53 R248W mutation created by TALEN-mediated precise gene editing. The H1-p53(R248W/R248W) cell line maintains a normal karyotype, robust pluripotency gene expression, and the potential to differentiate to the three germ layers.
Highlights
Genetic mutations in TP53 contribute to multiple human cancers
The H1-p53(R248W/R248W) line provides an ideal model for studying the functions of the p53(R248W) mutation in tumor initiation and progression in a human cell model, which opens up opportunities for development of new cancer therapeutic strategies
The targeting plasmids contain (1) a pair of Transcription activator-like effector nucleases (TALEN) plasmids targeting exon7 and intron 7 of TP53, respectively; and (2) a pFNF donor vector carrying a Frt-EM7-NeoR-Frt (FNF) selection cassette flanked by 1 kb left and right homologous arms of the TP53 genomic region
Summary
Genetic mutations in TP53 contribute to multiple human cancers. Here we report the generation of a H1-p53(R248W/R248W) human embryonic stem cell line harboring a homozygous TP53 R248W mutation created by TALEN-mediated precise gene editing. The H1-p53(R248W/R248W) line provides an ideal model for studying the functions of the p53(R248W) mutation in tumor initiation and progression in a human cell model, which opens up opportunities for development of new cancer therapeutic strategies. TP53 is the most mutated gene in human cancers and leads to tumor initiation and progression in multiple cell types (Zhou et al, 2017).
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