ArticleDevelopment (Cambridge, England)2022
TWIST1 interacts with β/δ-catenins during neural tube development and regulates fate transition in cranial neural crest cells.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- Cross-Modal Denoising and Integration of Spatial Multi-Omics Data with CANDIES.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Generation and Characterization of Twist1 Acetyl-Mimic and Acetyl-Deficient Mouse Models.Genesis (New York, N.Y. : 2000) · 2026Article
- δ-catenin controls layer-specific transcriptional maturation of astrocytes via Zbtb20.bioRxiv : the preprint server for biology · 2026Article
- Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors.Developmental biology · 2026Article
- Loss of Twist1 leads to disruption of ciliary length, endocytic vesicle dynamics, and cell-cell junctions during neural tube formation.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.Frontiers in physiology · 2026Article
- Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.bioRxiv : the preprint server for biology · 2025Article
- TWIST1 Modulates Cilia Length, Endocytic Vesicle Dynamics, and Cell-Cell Junctions during Neural Tube Morphogenesis.bioRxiv : the preprint server for biology · 2025Article
- IRF6 regulates adherens junction proteins and inflammatory cytokines in salivary acinar cells and its expression is elevated in Sjӧgren's syndrome.Archives of oral biology · 2025Article
- Opposite patterns of association of TWIST1 expression with patient survival in SHH and Group 4 medulloblastoma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Article
- Article
- Neural crest and periderm-specific requirements of Irf6 during neural tube and craniofacial development.Developmental biology · 2025Review
- Twist1 Acts Upstream of the Dlx5-Hand2 Pathway to Pattern the Mammalian Jaw.Journal of dental research · 2025Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- Neural crest and periderm-specific requirements ofbioRxiv : the preprint server for biology · 2024Article
- A novelFrontiers in genetics · 2024Article
- δ-catenin promotes Twist1 stabilization in prostate cancer through ubiquitination modification.American journal of cancer research · 2024Article
- SPECC1L: a cytoskeletal protein that regulates embryonic tissue dynamics.Biochemical Society transactions · 2023Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 4 countries.
Funding
Abstract
Cell fate determination is a necessary and tightly regulated process for producing different cell types and structures during development. Cranial neural crest cells (CNCCs) are unique to vertebrate embryos and emerge from the neural plate borders into multiple cell lineages that differentiate into bone, cartilage, neurons and glial cells. We have previously reported that Irf6 genetically interacts with Twist1 during CNCC-derived tissue formation. Here, we have investigated the mechanistic role of Twist1 and Irf6 at early stages of craniofacial development. Our data indicate that TWIST1 is expressed in endocytic vesicles at the apical surface and interacts with β/δ-catenins during neural tube closure, and Irf6 is involved in defining neural fold borders by restricting AP2α expression. Twist1 suppresses Irf6 and other epithelial genes in CNCCs during the epithelial-to-mesenchymal transition (EMT) process and cell migration. Conversely, a loss of Twist1 leads to a sustained expression of epithelial and cell adhesion markers in migratory CNCCs. Disruption of TWIST1 phosphorylation in vivo leads to epidermal blebbing, edema, neural tube defects and CNCC-derived structural abnormalities. Altogether, this study describes a previously uncharacterized function of mammalian Twist1 and Irf6 in the neural tube and CNCCs, and provides new target genes for Twist1 that are involved in cytoskeletal remodeling.
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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.