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Splice-altering TP53 missense mutations: Drivers of functional loss and therapeutic targets via RNA modulation

GSE297670 Homo sapiens Expression profiling by high throughput sequencing 18 samples 2026/05/31 GPL28038
Summary
Using bacterial artificial chromosome DNA-mediated targeting, we developed knock-in TP53 mutant cell models including c.182A>G, c.318C>G, c.356C>G and c.362C>A. These missense mutations can function as frameshift or hypomorphic mutations due to aberrant splicing, significantly compromising TP53 mRNA integrity.
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