ArticleLife science alliance2023
The ribose methylation enzyme FTSJ1 has a conserved role in neuron morphology and learning performance.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Global and specific mechanisms stimulate mistranslation in cancer.Nature cell biology · 2026Article
- Anticodon nucleotide modifications affect translational tuning by the ribosomal CAR surface.bioRxiv : the preprint server for biology · 2026Article
- Review
- Targeting tRNA methyltransferases: from molecular mechanisms to drug discovery.Science China. Life sciences · 2025Review
- Identification and validation of prognostic models and tumor microenvironment infiltration characteristics for tRNA modification regulators in clear cell renal cell carcinoma.Oncology letters · 2025Article
- Structural insights into tRNA recognition of the human FTSJ1-THADA complex.Communications biology · 2025Article
- RNA modification: a promising code to unravel the puzzle of autoimmune diseases and CD4Frontiers in immunology · 2025Review
- Unlocking the Gateway: The Spatio-Temporal Dynamics of the p53 Family Driven by the Nuclear Pores and Its Implication for the Therapeutic Approach in Cancer.International journal of molecular sciences · 2024Review
- Exploring the brain epitranscriptome: perspectives from the NSAS summit.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FTSJ1 is a conserved human 2'-O-methyltransferase (Nm-MTase) that modifies several tRNAs at position 32 and the wobble position 34 in the anticodon loop. Its loss of function has been linked to X-linked intellectual disability (XLID), and more recently to cancers. However, the molecular mechanisms underlying these pathologies are currently unclear. Here, we report a novel
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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.