| Literature DB >> 34260931 |
Chingakham Ranjit Singh1, M Rebecca Glineburg2, Chelsea Moore1, Naoki Tani3, Rahul Jaiswal4, Ye Zou5, Eric Aube1, Sarah Gillaspie1, Mackenzie Thornton1, Ariana Cecil1, Madelyn Hilgers1, Azuma Takasu1, Izumi Asano1, Masayo Asano1, Carlos R Escalante4, Akira Nakamura3, Peter K Todd6, Katsura Asano7.
Abstract
eIF5-mimic protein (5MP) is a translational regulatory protein that binds the small ribosomal subunit and modulates its activity. 5MP is proposed to reprogram non-AUG translation rates for oncogenes in cancer, but its role in controlling non-AUG initiated synthesis of deleterious repeat-peptide products, such as FMRpolyG observed in fragile-X-associated tremor ataxia syndrome (FXTAS), is unknown. Here, we show that 5MP can suppress both general and repeat-associated non-AUG (RAN) translation by a common mechanism in a manner dependent on its interaction with eIF3. Essentially, 5MP displaces eIF5 through the eIF3c subunit within the preinitiation complex (PIC), thereby increasing the accuracy of initiation. In Drosophila, 5MP/Kra represses neuronal toxicity and enhances the lifespan in an FXTAS disease model. These results implicate 5MP in protecting cells from unwanted byproducts of non-AUG translation in neurodegeneration.Entities:
Keywords: FXTAS; RAN translation; cancer; eIF5-mimic protein; non-AUG start codon; ribosome; translation initiation
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Year: 2021 PMID: 34260931 PMCID: PMC8363759 DOI: 10.1016/j.celrep.2021.109376
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423