ArticleFEBS letters2013
Slow growth and unstable ribosomal RNA lacking pseudouridine in mouse embryonic fibroblast cells expressing catalytically inactive dyskerin.
Article in FEBS letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- RNA modifications in cancer.MedComm · 2025Review
- SNORA14A inhibits hepatoblastoma cell proliferation by regulating SDHB-mediated succinate metabolism.Cell death discovery · 2023Article
- The role of RNA modification in hepatocellular carcinoma.Frontiers in pharmacology · 2022Review
- The role of mMolecular cancer · 2021Review
- snoRNPs: Functions in Ribosome Biogenesis.Biomolecules · 2020Review
- A ribosome-related signature in peripheral blood CLL B cells is linked to reduced survival following treatment.Cell death & disease · 2016Article
- Article
- The dyskerin ribonucleoprotein complex as an OCT4/SOX2 coactivator in embryonic stem cells.eLife · 2014Article
- Mutation of EMG1 causing Bowen-Conradi syndrome results in reduced cell proliferation rates concomitant with G2/M arrest and 18S rRNA processing delay.BBA clinical · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pseudouridine is the most abundant modified nucleotide in ribosomal RNA throughout eukaryotes and archaea but its role is not known. Here we produced mouse embryonic fibroblast cells expressing only catalytically inactive dyskerin, the pseudouridine synthase that converts uridine to pseudouridine in ribosomal RNA. The mutant dyskerin protein, D125A, was extremely unstable but cells were able to divide and grow very slowly. Abnormalities in ribosome RNA synthesis were apparent but mature cytoplasmic RNAs lacking pseudouridine were produced and were very unstable. We conclude that pseudouridine is required to stabilize the secondary structure of ribosomal RNA that is essential for its function.
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Registered trials
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