ArticleCell reports2019
Widespread Alterations in Translation Elongation in the Brain of Juvenile Fmr1 Knockout Mice.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 80 citations in OpenAlex.
- CB1 receptor inhibition restores synaptoneurosomal alternative splicing landscape in fragile X syndrome mice.iScience · 2026Article
- Correction of eIF4E overactivation rescues translatome imbalance and core ASD-like behaviors in valproic acid-induced offspring mice.Molecular psychiatry · 2026Article
- FMRP drives mRNP targets into translationally silenced complexes.Molecular cell · 2025Article
- Article
- Dysregulated ribosome quality control in human diseases.The FEBS journal · 2025Review
- Trinucleotide repeat expansion and RNA dysregulation in fragile X syndrome: emerging therapeutic approaches.RNA (New York, N.Y.) · 2025Review
- Construction destruction: Contribution of dyregulated proteostasis to neurodevelopmental disorders.Current opinion in neurobiology · 2025Review
- Glioma-Induced Alterations in Excitatory Neurons are Reversed by mTOR Inhibition.bioRxiv : the preprint server for biology · 2024Article
- Crosstalk between ubiquitination and translation in neurodevelopmental disorders.Frontiers in molecular neuroscience · 2024Review
- FMRP deficiency leads to multifactorial dysregulation of splicing and mislocalization of MBNL1 to the cytoplasm.PLoS biology · 2023Article
- Article
- Cell-type-specific disruption of cortico-striatal circuitry drives repetitive patterns of behavior in fragile X syndrome model mice.Cell reports · 2023Article
- Antisense oligonucleotide rescue of CGG expansion-dependentProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Comparative oxidation proteomics analyses suggest redox regulation of cytosolic translation in rice leaves upon Magnaporthe oryzae infection.Plant communications · 2023Article
- Alterations in oligodendrocyte transcriptional networks reveal region-specific vulnerabilities to neurological disease.iScience · 2023Article
- RPL3L-containing ribosomes determine translation elongation dynamics required for cardiac function.Nature communications · 2023Article
- choros: correction of sequence-based biases for accurate quantification of ribosome profiling data.bioRxiv : the preprint server for biology · 2023Article
- Impaired synaptic incorporation of AMPA receptors in a mouse model of fragile X syndrome.Frontiers in molecular neuroscience · 2023Article
- Article
- Excess ribosomal protein production unbalances translation in a model of Fragile X Syndrome.Nature communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
FMRP (fragile X mental retardation protein) is a polysome-associated RNA-binding protein encoded by Fmr1 that is lost in fragile X syndrome. Increasing evidence suggests that FMRP regulates both translation initiation and elongation, but the gene specificity of these effects is unclear. To elucidate the impact of Fmr1 loss on translation, we utilize ribosome profiling for genome-wide measurements of ribosomal occupancy and positioning in the cortex of 24-day-old Fmr1 knockout mice. We find a remarkably coherent reduction in ribosome footprint abundance per mRNA for previously identified, high-affinity mRNA binding partners of FMRP and an increase for terminal oligopyrimidine (TOP) motif-containing genes canonically controlled by mammalian target of rapamycin-eIF4E-binding protein-eIF4E binding protein-eukaryotic initiation factor 4E (mTOR-4E-BP-eIF4E) signaling. Amino acid motif- and gene-level analyses both show a widespread reduction of translational pausing in Fmr1 knockout mice. Our findings are consistent with a model of FMRP-mediated regulation of both translation initiation through eIF4E and elongation that is disrupted in fragile X syndrome.
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.