ArticleProceedings of the National Academy of Sciences of the United States of America2014
Upregulation of eIF5B controls cell-cycle arrest and specific developmental stages.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
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- Start codon-associated ribosomal frameshifting mediates nutrient stress adaptation.Nature structural & molecular biology · 2023Article
- Review
- Ribosome changes reprogram translation for chemosurvival in G0 leukemic cells.Science advances · 2022Article
- IGF2BP3-induced activation of EIF5B contributes to progression of hepatocellular carcinoma cells.Oncology research · 2022Article
- Depletion of eukaryotic initiation factor 5B (eIF5B) reprograms the cellular transcriptome and leads to activation of endoplasmic reticulum (ER) stress and c-Jun N-terminal kinase (JNK).Cell stress & chaperones · 2021Article
- Established and Emerging Regulatory Roles of Eukaryotic Translation Initiation Factor 5B (eIF5B).Frontiers in genetics · 2021Review
- Dynamics of protein synthesis in the initial steps of strobilation in the model cestode parasite Mesocestoides corti (syn. vogae).Journal of proteomics · 2020Article
- Identification of GSN and LAMC2 as Key Prognostic Genes of Bladder Cancer by Integrated Bioinformatics Analysis.Cancers · 2020Article
- A post-transcriptional program of chemoresistance by AU-rich elements and TTP in quiescent leukemic cells.Genome biology · 2020Article
- Understanding the role of calcium-mediated cell death in high-frequency irreversible electroporation.Bioelectrochemistry (Amsterdam, Netherlands) · 2020Article
- Long-range interdomain communications in eIF5B regulate GTP hydrolysis and translation initiation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Eukaryotic initiation factor 5B (eIF5B) provides a critical cell survival switch to glioblastoma cells via regulation of apoptosis.Cell death & disease · 2019Article
- Eukaryotic Initiation Factor 5B (eIF5B) Cooperates with eIF1A and eIF5 to Facilitate uORF2-Mediated Repression of ATF4 Translation.International journal of molecular sciences · 2018Article
- Article
- Analysis of MicroRNA-Mediated Translation Activation of In Vitro Transcribed Reporters in Quiescent Cells.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Mutations in eIF5B Confer Thermosensitive and Pleiotropic Phenotypes via Translation Defects inThe Plant cell · 2017Article
- FXR1a-associated microRNP: A driver of specialized non-canonical translation in quiescent conditions.RNA biology · 2017Review
- Article
- Regulation of monocyte induced cell migration by the RNA binding protein, FXR1.Cell cycle (Georgetown, Tex.) · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proliferation arrest and distinct developmental stages alter and decrease general translation yet maintain ongoing translation. The factors that support translation in these conditions remain to be characterized. We investigated an altered translation factor in three cell states considered to have reduced general translation: immature Xenopus laevis oocytes, mouse ES cells, and the transition state of proliferating mammalian cells to quiescence (G0) upon growth-factor deprivation. Our data reveal a transient increase of eukaryotic translation initiation factor 5B (eIF5B), the eukaryotic ortholog of bacterial initiation factor IF2, in these conditions. eIF5B promotes 60S ribosome subunit joining and pre-40S subunit proofreading. eIF5B has also been shown to promote the translation of viral and stress-related mRNAs and can contribute indirectly to supporting or stabilizing initiator methionyl tRNA (tRNA-Met(i)) association with the ribosome. We find that eIF5B is a limiting factor for translation in these three conditions. The increased eIF5B levels lead to increased eIF5B complexes with tRNA-Met(i) upon serum starvation of THP1 mammalian cells. In addition, increased phosphorylation of eukaryotic initiation factor 2α, the translation factor that recruits initiator tRNA-Meti for general translation, is observed in these conditions. Importantly, we find that eIF5B is an antagonist of G0 and G0-like states, as eIF5B depletion reduces maturation of G0-like, immature oocytes and hastens early G0 arrest in serum-starved THP1 cells. Consistently, eIF5B overexpression promotes maturation of G0-like immature oocytes and causes cell death, an alternative to G0, in serum-starved THP1 cells. These data reveal a critical role for a translation factor that regulates specific cell-cycle transition and developmental stages.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.