ArticleMolecular cell2023
FMRP phosphorylation modulates neuronal translation through YTHDF1.
Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 76 citations in OpenAlex.
- The YTHDF proteins modulate Alzheimer's disease-associated brain gene signatures.Molecular neurodegeneration · 2026Article
- METTL14-Mediated N6-Methyladenosine Exacerbates Acute Lung Injury via USP30/NCOA4-Dependent Ferroptosis.MedComm · 2026Article
- mNature reviews. Neuroscience · 2026Review
- The mMolecular psychiatry · 2026Article
- The m⁶A reader YTHDF2 regulates mRNA transport and axon outgrowth in developing neurons.Nature communications · 2026Article
- RNA modifications and epigenetic regulation in plants.aBIOTECH · 2026Review
- Regulatory elements on chromatin-associated RNA 15 years beyond RNA epigenetics.Nature chemical biology · 2026Review
- The Role of NMedComm · 2026Review
- Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026Review
- RNA‑binding proteins as epithelial transcriptome orchestrators in gastric cancer: Immune‑metabolic crosstalk and therapeutic vulnerability (Review).International journal of molecular medicine · 2026Review
- The choreography of development: RNA localization across time and space.Development (Cambridge, England) · 2026Review
- The RNA methylation modification as an immunometabolic regulatory hub in pancreatic cancer: from mechanistic insights to clinical translation perspectives.Molecular cancer · 2026Review
- mRNA mProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mechanisms and therapeutic potential of YTHDF readers: Linking epitranscriptomics to cancer.Journal of pharmaceutical analysis · 2026Review
- Human organoids as 3D in vitro platforms for drug discovery: opportunities and challenges.Nature reviews. Drug discovery · 2026Review
- Engineering a human-based translational activator for targeted protein expression restoration.Nucleic acids research · 2026Article
- Deep learning-assisted discovery of a potent and cell-active inhibitor of RNA NNature communications · 2026Article
- Microglial Sestrin2 alleviates depressive-like behaviors and cognitive impairment in a YTHDF1-dependent manner.Frontiers in neuroscience · 2026Article
- RNA modification systems as therapeutic targets.Nature reviews. Drug discovery · 2026Review
- RNA modifications in cancer: from biological insights to therapeutic targets.Bioorganic & medicinal chemistry · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
RNA-binding proteins (RBPs) control messenger RNA fate in neurons. Here, we report a mechanism that the stimuli-induced neuronal translation is mediated by phosphorylation of a YTHDF1-binding protein FMRP. Mechanistically, YTHDF1 can condense with ribosomal proteins to promote the translation of its mRNA targets. FMRP regulates this process by sequestering YTHDF1 away from the ribosome; upon neuronal stimulation, FMRP becomes phosphorylated and releases YTHDF1 for translation upregulation. We show that a new small molecule inhibitor of YTHDF1 can reverse fragile X syndrome (FXS) developmental defects associated with FMRP deficiency in an organoid model. Our study thus reveals that FMRP and its phosphorylation are important regulators of activity-dependent translation during neuronal development and stimulation and identifies YTHDF1 as a potential therapeutic target for FXS in which developmental defects caused by FMRP depletion could be reversed through YTHDF1 inhibition.
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.