ArticleNature communications2016
Prevention of Treacher Collins syndrome craniofacial anomalies in mouse models via maternal antioxidant supplementation.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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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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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- The association between maternal smoking during pregnancy and dental development in offspring: a systematic review.Evidence-based dentistry · 2025Pooled it
- Unveiling the Prevalence and Surgical Burden of Neurocristopathies: A Scoping Review and Statistical Analysis.Research square · 2026Article
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- TCOF1 Regulates Tumor Cell Migration Through p53-Dependent Mitochondrial Homeostasis and F-Actin Dynamics.Current issues in molecular biology · 2026Article
- NR6A1 is essential for neural crest cell specification, formation and survival.Nature communications · 2026Article
- Analysis of the clinical features of neurocristopathy-related hearing loss and how these relate to outcomes after cochlear implantation.Scientific reports · 2025Article
- Is mitochondrial function at the heart of ribosome-related diseases?Trends in cell biology · 2025Review
- Gene-environment interactions modulate the phenotype severity in mouse models of congenital craniofacial syndromes.The Journal of clinical investigation · 2025Article
- Article
- Deciphering TCOF1 mutations in Chinese Treacher Collins syndrome patients: insights into pathogenesis and transcriptional disruption.Orphanet journal of rare diseases · 2025Article
- Oxidative stress-mediated apoptosis via theFrontiers in pediatrics · 2025Article
- Early increased cell proliferation compensates subsequent hypoplasia of the ossicle.Frontiers in cell and developmental biology · 2025Article
- Maternal antioxidant treatment partially rescues developmental defects in amicroPublication biology · 2025Article
- Vascular architecture regulates mesenchymal stromal cell heterogeneity via P53-PDGF signaling in the mouse incisor.Cell stem cell · 2024Article
- The transcription of the main gene associated with Treacher-Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP).Scientific reports · 2024Article
- Recapitulating and reversing human brain ribosomopathy defects via the maladaptive integrated stress response.Science advances · 2024Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
- Glycolytic activity is required for the onset of neural plate folding during neural tube closure in mouse embryos.Frontiers in cell and developmental biology · 2023Article
- A clinically-relevant residue of POLR1D is required for Drosophila development.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Disrupted tenogenesis in masseter as a potential cause of micrognathia.International journal of oral science · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Craniofacial anomalies account for approximately one-third of all birth defects and are a significant cause of infant mortality. Since the majority of the bones, cartilage and connective tissues that comprise the head and face are derived from a multipotent migratory progenitor cell population called the neural crest, craniofacial disorders are typically attributed to defects in neural crest cell development. Treacher Collins syndrome (TCS) is a disorder of craniofacial development and although TCS arises primarily through autosomal dominant mutations in TCOF1, no clear genotype-phenotype correlation has been documented. Here we show that Tcof1 haploinsufficiency results in oxidative stress-induced DNA damage and neuroepithelial cell death. Consistent with this discovery, maternal treatment with antioxidants minimizes cell death in the neuroepithelium and substantially ameliorates or prevents the pathogenesis of craniofacial anomalies in Tcof1(+/-) mice. Thus maternal antioxidant dietary supplementation may provide an avenue for protection against the pathogenesis of TCS and similar neurocristopathies.
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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.