ArticlePLoS genetics2017
The T-cell leukemia related rpl10-R98S mutant traps the 60S export adapter Nmd3 in the ribosomal P site in yeast.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- From ribosomopathies to therapeutic targets: ribosomal alterations in pediatric leukemogenesis and tumorigenesis.Frontiers in oncology · 2026Review
- ZNF574 is a quality control factor for defective ribosome biogenesis intermediates.Molecular cell · 2025Article
- The assembly factor Reh1 is released from the ribosome during its initial round of translation.Nature communications · 2025Article
- Quality control ensures fidelity in ribosome assembly and cellular health.The Journal of cell biology · 2023Review
- Dynamic states of eIF6 and SDS variants modulate interactions with uL14 of the 60S ribosomal subunit.Nucleic acids research · 2023Article
- Panels of mRNAs and miRNAs for decoding molecular mechanisms of Renal Cell Carcinoma (RCC) subtypes utilizing Artificial Intelligence approaches.Scientific reports · 2022Article
- Genetics animates structure: leveraging genetic interactions to study the dynamics of ribosome biogenesis.Current genetics · 2021Review
- Review
- Regulation of eukaryotic translation initiation factor 6 dynamics through multisite phosphorylation by GSK3.The Journal of biological chemistry · 2020Article
- From Snapshots to Flipbook-Resolving the Dynamics of Ribosome Biogenesis with Chemical Probes.International journal of molecular sciences · 2020Review
- Ribosomal protein gene RPL9 variants can differentially impair ribosome function and cellular metabolism.Nucleic acids research · 2020Article
- Article
- Tightly-orchestrated rearrangements govern catalytic center assembly of the ribosome.Nature communications · 2019Article
- Article
- Ribosomal protein L10 in mitochondria serves as a regulator for ROS level in pancreatic cancer cells.Redox biology · 2018Article
- Molecular basis of the human ribosomopathy Shwachman-Diamond syndrome.Advances in biological regulation · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the ribosomal protein Rpl10 (uL16) can be drivers of T-cell acute lymphoblastic leukemia (T-ALL). We previously showed that these T-ALL mutations disrupt late cytoplasmic maturation of the 60S ribosomal subunit, blocking the release of the trans-acting factors Nmd3 and Tif6 in S. cerevisiae. Consequently, these mutant ribosomes do not efficiently pass the cytoplasmic quality control checkpoint and are blocked from engaging in translation. Here, we characterize suppressing mutations of the T-ALL-related rpl10-R98S mutant that bypass this block and show that the molecular defect of rpl10-R98S is a failure to release Nmd3 from the P site. Suppressing mutations were identified in Nmd3 and Tif6 that disrupted interactions between Nmd3 and the ribosome, or between Nmd3 and Tif6. Using an in vitro system with purified components, we found that Nmd3 inhibited Sdo1-stimulated Efl1 activity on mutant rpl10-R98S but not wild-type 60S subunits. Importantly, this inhibition was overcome in vitro by mutations in Nmd3 that suppressed rpl10-R98S in vivo. These results strongly support a model that Nmd3 must be dislodged from the P site to allow Sdo1 activation of Efl1, and define a failure in the removal of Nmd3 as the molecular defect of the T-ALL-associated rpl10-R98S mutation.
Indexed as
Identifiers
What OpenQuestion holds
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.