Adding to the CASeload: unwarranted p53 signaling induced by Cas9

Cas9 诱导的 p53 信号传导异常,进一步加重了 CASeload 的负担。

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Abstract

We investigated the genetic and transcriptional changes associated with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated protein 9 (Cas9) expression in human cancer cell lines. For a subset of cell lines with a wild-type tumor protein TP53 (best known as p53), we detected p53 pathway activation, DNA damage accumulation and emerging p53-inactivating mutations following Cas9 introduction. We discuss the potential implications of our findings in basic and translational research.

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