A CRISPR/dCasX‐mediated transcriptional programming system for inhibiting the progression of bladder cancer cells by repressing c‐MYC or activating TP53

摘要

The CRISPR-associated catalytically inactive SpdCas9 and,withdistinct regulatory functions enables stable and efficient transcrip- tional repression or activation. 1–4 Recently, DpbCas12e protein (formerly CasX) from Deltaproteobacteria forms a distinct subtype of Class II type V CRISPR-Cas effectors and can introduce programmable double-stranded breaks in mammalian genomes. 5 Here, we identify that fusions of the nuclease-inactive dead CasX (dCasX) to the KRAB repressor (dCasX-KRAB) or VPR activator (dCasX-VPR) can silence or activate target gene expression in human cells.