Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112-5650, USA.
Trends Pharmacol Sci. 2018 Sep;39(9):783-784. doi: 10.1016/j.tips.2018.06.005. Epub 2018 Jul 11.
The efficacy of the powerful CRISPR-Cas9 genome-editing platform depends on DNA repair activities in the cells being targeted. Two new papers show that the low efficiency of targeting in some primary human cell lines is the result of p53-dependent cell arrest in response to the Cas9-induced break. This limitation must be overcome for some anticipated therapies.
强大的 CRISPR-Cas9 基因组编辑平台的功效取决于目标细胞中的 DNA 修复活动。两篇新论文表明，某些原代人细胞系靶向效率低的原因是 Cas9 诱导的断裂导致 p53 依赖性细胞停滞。对于一些预期的治疗方法，必须克服这一限制。
