ReviewDevelopment, growth & differentiation2016
Face off against ROS: Tcof1/Treacle safeguards neuroepithelial cells and progenitor neural crest cells from oxidative stress during craniofacial development.
Review in Development, growth & differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 67 citations in OpenAlex.
- Novel TCOF1 Frameshift Variant and Phenotypic Heterogeneity in a Chinese Family With Treacher Collins Syndrome.Molecular genetics & genomic medicine · 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
- TCOF1 affects Golgi secretory pathway contributing to the angiogenesis in renal cancer.Cell communication and signaling : CCS · 2026Article
- Genetic and Molecular Characterization of Treacher Collins Syndrome in Three Mexican Families.International journal of molecular sciences · 2026Article
- 3D biomimetic niche modulates embryo development in vitro.Nature communications · 2026Article
- Gene-environment interactions modulate the phenotype severity in mouse models of congenital craniofacial syndromes.The Journal of clinical investigation · 2025Article
- Case Report: A novel heterozygous variant of theFrontiers in pediatrics · 2025Article
- Alterations of senescence-associated markers in patients with non-syndromic cleft lip and palate.Scientific reports · 2024Article
- Etiology of craniofacial and cardiac malformations in a mouse model ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Apoptotic metabolites ameliorate bone aging phenotypes via TCOF1/FLVCR1-mediated mitochondrial homeostasis.Journal of nanobiotechnology · 2024Article
- Article
- Two novel pathogenic variants in the TCOF1 found in two Chinese cases of Treacher Collins syndrome.Molecular genetics & genomic medicine · 2024Article
- Identification and characterization of intermediate states in mammalian neural crest cell epithelial to mesenchymal transition and delamination.bioRxiv : the preprint server for biology · 2024Article
- rRNA transcription is integral to phase separation and maintenance of nucleolar structure.PLoS genetics · 2023Article
- Cyclophilin A as a Pro-Inflammatory Factor Exhibits Embryotoxic and Teratogenic Effects during Fetal Organogenesis.International journal of molecular sciences · 2023Article
- Augmentation of bone morphogenetic protein signaling in cranial neural crest cells in mice deforms skull base due to premature fusion of intersphenoidal synchondrosis.Genesis (New York, N.Y. : 2000) · 2023Article
- RNA Polymerases I and III in development and disease.Seminars in cell & developmental biology · 2023Review
- BMP signaling during craniofacial development: new insights into pathological mechanisms leading to craniofacial anomalies.Frontiers in physiology · 2023Review
- Dynamic regulation and requirement for ribosomal RNA transcription during mammalian development.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
One-third of all congenital birth defects affect the head and face, and most craniofacial anomalies are considered to arise through defects in the development of cranial neural crest cells. Cranial neural crest cells give rise to the majority of craniofacial bones, cartilages and connective tissues. Therefore, understanding the events that control normal cranial neural crest and subsequent craniofacial development is important for elucidating the pathogenetic mechanisms of craniofacial anomalies and for the exploring potential therapeutic avenues for their prevention. Treacher Collins syndrome (TCS) is a congenital disorder characterized by severe craniofacial anomalies. An animal model of TCS, generated through mutation of Tcof1, the mouse (Mus musculus) homologue of the gene primarily mutated in association with TCS in humans, has recently revealed significant insights into the pathogenesis of TCS. Apoptotic elimination of neuroepithelial cells including neural crest cells is the primary cause of craniofacial defects in Tcof1 mutant embryos. However, our understanding of the mechanisms that induce tissue-specific apoptosis remains incomplete. In this review, we describe recent advances in our understanding of the pathogenesis TCS. Furthermore, we discuss the role of Tcof1 in normal embryonic development, the correlation between genetic and environmental factors on the severity of craniofacial abnormalities, and the prospect for prenatal prevention of craniofacial anomalies.
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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.