无意义介导的衰变
生物
基因组编辑
基因
免疫疗法
无义突变
疾病
Cas9
基因组
突变
清脆的
计算生物学
癌症研究
遗传学
癌症
胡说
核糖核酸
医学
RNA剪接
病理
错义突变
作者
Rik G.H. Lindeboom,Michiel Vermeulen,Ben Lehner,Fran Supek
出处
期刊:Nature Genetics
[Nature Portfolio]
日期:2019-10-28
卷期号:51 (11): 1645-1651
被引量:338
标识
DOI:10.1038/s41588-019-0517-5
摘要
Premature termination codons (PTCs) can result in the production of truncated proteins or the degradation of messenger RNAs by nonsense-mediated mRNA decay (NMD). Which of these outcomes occurs can alter the effect of a mutation, with the engagement of NMD being dependent on a series of rules. Here, by applying these rules genome-wide to obtain a resource called NMDetective, we explore the impact of NMD on genetic disease and approaches to therapy. First, human genetic diseases differ in whether NMD typically aggravates or alleviates the effects of PTCs. Second, failure to trigger NMD is a cause of ineffective gene inactivation by CRISPR-Cas9 gene editing. Finally, NMD is a determinant of the efficacy of cancer immunotherapy, with only frameshifted transcripts that escape NMD predicting a response. These results demonstrate the importance of incorporating the rules of NMD into clinical decision-making. Moreover, they suggest that inhibiting NMD may be effective in enhancing cancer immunotherapy.
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