Translation arrest as a protein quality control system for aberrant translation of the 3'-UTR in mammalian cells.

Abstract:

:Read-through or mutations of a stop codon resulting in translation of the 3'-UTR produce potentially toxic C-terminally extended proteins. However, quality control mechanisms for such proteins are poorly understood in mammalian cells. Here, a comprehensive analysis of the 3'-UTRs of genes associated with hereditary diseases identified novel arrest-inducing sequences in the 3'-UTRs of 23 genes that can repress the levels of their protein products. In silico analysis revealed that the hydrophobicity of the polypeptides encoded in the 3'-UTRs is correlated with arrest efficiency. These results provide new insight into quality control mechanisms mediated by 3'-UTRs to prevent the production of C-terminally extended cytotoxic proteins.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Hashimoto S,Nobuta R,Izawa T,Inada T

doi

10.1002/1873-3468.13362

subject

Has Abstract

pub_date

2019-04-01 00:00:00

pages

777-787

issue

8

eissn

0014-5793

issn

1873-3468

journal_volume

593

pub_type

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