ArticleMolecular and cellular biology2005
Involvement of human release factors eRF3a and eRF3b in translation termination and regulation of the termination complex formation.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 91 citations in OpenAlex.
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- Human Tissues Exhibit Diverse Composition of Translation Machinery.International journal of molecular sciences · 2023Article
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- Features and factors that dictate if terminating ribosomes cause or counteract nonsense-mediated mRNA decay.The Journal of biological chemistry · 2022Review
- Small-molecule eRF3a degraders rescue CFTR nonsense mutations by promoting premature termination codon readthrough.The Journal of clinical investigation · 2022Article
- Proximity interactome analysis of Lassa polymerase reveals eRF3a/GSPT1 as a druggable target for host-directed antivirals.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Tissue-specific regulation of translational readthrough tunes functions of the traffic jam transcription factor.Nucleic acids research · 2022Article
- 4210 Da and 1866 Da polypeptides as potential biomarkers of liver disease progression in hepatitis B virus patients.Scientific reports · 2021Article
- Identification of a Locus on the X Chromosome Linked to Familial Membranous Nephropathy.Kidney international reports · 2021Article
- Effect of small molecule eRF3 degraders on premature termination codon readthrough.Nucleic acids research · 2021Article
- Identification and activity of the functional complex between hnRNPL and the pseudoexfoliation syndrome-associated lncRNA, LOXL1-AS1.Human molecular genetics · 2020Article
- Translational recoding: canonical translation mechanisms reinterpreted.Nucleic acids research · 2020Review
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- Further Clinical and Molecular Delineation of Xp11.22 Deletion Syndrome: A Case Report.Oman medical journal · 2019Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
eRF3 is a GTPase associated with eRF1 in a complex that mediates translation termination in eukaryotes. In mammals, two genes encode two distinct forms of eRF3, eRF3a and eRF3b, which differ in their N-terminal domains. Both bind eRF1 and stimulate its release activity in vitro. However, whether both proteins can function as termination factors in vivo has not been determined. In this study, we used short interfering RNAs to examine the effect of eRF3a and eRF3b depletion on translation termination efficiency in human cells. By measuring the readthrough at a premature nonsense codon in a reporter mRNA, we found that eRF3a silencing induced an important increase in readthrough whereas eRF3b silencing had no significant effect. We also found that eRF3a depletion reduced the intracellular level of eRF1 protein by affecting its stability. In addition, we showed that eRF3b overexpression alleviated the effect of eRF3a silencing on readthrough and on eRF1 cellular levels. These results suggest that eRF3a is the major factor acting in translation termination in mammals and clearly demonstrate that eRF3b can substitute for eRF3a in this function. Finally, our data indicate that the expression level of eRF3a controls the formation of the termination complex by modulating eRF1 protein stability.
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