ArticleCell2017
Excess Translation of Epigenetic Regulators Contributes to Fragile X Syndrome and Is Alleviated by Brd4 Inhibition.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 126 citations in OpenAlex.
- Article
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Whole-genome 3D architectural screen reveals modulators of brain DNA structure.bioRxiv : the preprint server for biology · 2026Article
- Metabolic reprogramming during human neuron differentiation indicates glutaminase as a key determinant in Fragile X syndrome.Cell reports · 2026Article
- Age- and cell-type-specific effects of histone variant H2BE in the brain.Cell reports · 2025Article
- IGF2BPs directly regulate the noncanonical translation of toxic proteins from mutant FMR1 mRNA containing expanded CGG repeats.Nature communications · 2025Article
- Multiplexed smFISH Reveals the Spatial Organization of Neuropil Localized mRNAs Is Linked to Abundance.eNeuro · 2025Article
- Stress-Induced Membraneless Organelles in Neurons: Bridging Liquid-Liquid Phase Separation and Neurodevelopmental Dysfunction.International journal of molecular sciences · 2025Review
- Epigenetic Dysregulation in Neurodegenerative Disease: Implications for Neuropathology and Therapy.Cureus · 2025Review
- Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons.iScience · 2025Article
- Article
- Epigenetic modulation rescues neurodevelopmental deficits in Syngap1Aging cell · 2025Article
- Opto-CLIP reveals dynamic FMRP regulation of mRNAs upon CA1 neuronal activation.bioRxiv : the preprint server for biology · 2025Article
- Deep functional measurements of Fragile X syndrome human neurons reveal multiparametric electrophysiological disease phenotype.Communications biology · 2024Article
- Master regulators of neurogenesis: the dynamic roles of Ephrin receptors across diverse cellular niches.Translational psychiatry · 2024Review
- Histone variant H2BE enhances chromatin accessibility in neurons to promote synaptic gene expression and long-term memory.Molecular cell · 2024Article
- Histone variant H2BE enhances chromatin accessibility in neurons to promote synaptic gene expression and long-term memory.bioRxiv : the preprint server for biology · 2024Article
- Remodeling of the postsynaptic proteome in male mice and marmosets during synapse development.Nature communications · 2024Article
- Epigenetic insights into Fragile X Syndrome.Frontiers in cell and developmental biology · 2024Review
- Spatially coordinated heterochromatinization of long synaptic genes in fragile X syndrome.Cell · 2023Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Fragile X syndrome (FXS) is a leading genetic cause of intellectual disability and autism. FXS results from the loss of function of fragile X mental retardation protein (FMRP), which represses translation of target transcripts. Most of the well-characterized target transcripts of FMRP are synaptic proteins, yet targeting these proteins has not provided effective treatments. We examined a group of FMRP targets that encode transcriptional regulators, particularly chromatin-associated proteins. Loss of FMRP in mice results in widespread changes in chromatin regulation and aberrant gene expression. To determine if targeting epigenetic factors could reverse phenotypes associated with the disorder, we focused on Brd4, a BET protein and chromatin reader targeted by FMRP. Inhibition of Brd4 function alleviated many of the phenotypes associated with FXS. We conclude that loss of FMRP results in significant epigenetic misregulation and that targeting transcription via epigenetic regulators like Brd4 may provide new treatments for FXS.
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.