Factors Affecting Readthrough of Natural Versus Premature Termination Codons

Avigail Beryozkin, Kerstin Nagel-Wolfum, Eyal Banin, Dror Sharon*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

2 Scopus citations

Abstract

Nonsense mutations occur within the open-reading frame of a gene resulting in a premature termination codon (PTC). PTC-containing mRNAs can either be degeraded or cause premature translation termination producing a truncated protein that can be either nonfunctional or toxic. Translational readthrough inducing drugs (TRIDs) are small molecules that are able to induce readthrough, resulting in the restoration of full-length protein expression. The re-expressed proteins usually harbor a missense change. The effciency of individual TRIDs is variable and varies between different genes and even different nonsense mutations in the same gene. This review summarizes factors, including the sequences located upstream and downstream the disease-causing mutation and the type of PTC, affecting the translational readthrough process by modulating the type of amino acid insertion and the efficiency of the process during readthrough following TRIDs treatments.

Original languageEnglish
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer
Pages149-155
Number of pages7
DOIs
StatePublished - 2023

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1415
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Bibliographical note

Publisher Copyright:
© 2023, The Author(s), under exclusive license to Springer Nature Switzerland AG.

Keywords

  • Inherited retinal diseases
  • Nonsense mutations
  • Stop codons
  • Translation termination
  • Translational readthrough

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