平移移码
移码突变
生物
核糖体
翻译(生物学)
基因
核糖体RNA
计算生物学
机制(生物学)
遗传学
细胞生物学
信使核糖核酸
核糖核酸
突变
哲学
认识论
作者
Julien Champagne,Kelly Mordente,Remco Nagel,Reuven Agami
标识
DOI:10.1016/j.tig.2022.05.009
摘要
Programmed ribosomal frameshifting (PRF) is a key mechanism that viruses use to generate essential proteins for replication, and as a means of regulating gene expression. PRF generally involves recoding signals or frameshift stimulators to elevate the occurrence of frameshifting at shift-prone 'slippery' sequences. Given its essential role in viral replication, targeting PRF was envisioned as an attractive tool to block viral infection. However, in contrast to controlled-PRF mechanisms, recent studies have shown that ribosomes of many human cancer cell types are prone to frameshifting upon amino acid shortage; thus, these cells are deemed to be sloppy. The resulting products of a sloppy frameshift at the 'hungry' codons are aberrant proteins the degradation and display of which at the cell surface can trigger T cell activation. In this review, we address recent discoveries in ribosomal frameshifting and their functional consequences for the proteome in human cancer cells.
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