ArticleJournal of cell science2017
Cell-cycle-dependent TGFβ-BMP antagonism regulates neural tube closure by modulating tight junctions.
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Back to the Future-A 50-Year Dive into Embryo Implantation Research: Cell Biological Paradox, Epithelial Cell Polarity, and EMT.Biomolecules · 2026Review
- Changes in Epithelial Cell Polarity and Adhesion Guide Human Endometrial Receptivity: How In Vitro Systems Help to Untangle Mechanistic Details.Biomolecules · 2025Review
- Temporal morphogen gradient-driven neural induction shapes single expanded neuroepithelium brain organoids with enhanced cortical identity.Nature communications · 2023Article
- Distinct H3K27me3 and H3K27ac Modifications in Neural Tube Defects Induced by Benzo[a]pyrene.Brain sciences · 2023Article
- BMP/Smad Pathway Is Involved in Lithium Carbonate-Induced Neural-Tube Defects in Mice and Neural Stem Cells.International journal of molecular sciences · 2022Article
- Pathogenesis of neural tube defects: The regulation and disruption of cellular processes underlying neural tube closure.WIREs mechanisms of disease · 2022Review
- The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Review
- Article
- A Micropatterned Human-Specific Neuroepithelial Tissue for Modeling Gene and Drug-Induced Neurodevelopmental Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- An ontology for developmental processes and toxicities of neural tube closure.Reproductive toxicology (Elmsford, N.Y.) · 2021Article
- Uterine double-conditional inactivation ofProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies.Journal of developmental biology · 2018Review
- The cellular bases of choroid fissure formation and closure.Developmental biology · 2018Article
- Folate action in nervous system development and disease.Developmental neurobiology · 2018Review
- Morphogenetic defects underlie Superior Coloboma, a newly identified closure disorder of the dorsal eye.PLoS genetics · 2018Article
- Neural tube closure: cellular, molecular and biomechanical mechanisms.Development (Cambridge, England) · 2017Review
- Switching the rate and pattern of cell division for neural tube closure.Neurogenesis (Austin, Tex.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Many organs form by invaginating and rolling flat epithelial cell sheets into tubes. Invagination of the ventral midline of the neural plate forms the median hinge point (MHP), an event that elevates the neural folds and is essential for neural tube closure (NTC). MHP formation involves dynamic spatiotemporal modulations of cell shape, but how these are achieved is not understood. Here, we show that cell-cycle-dependent BMP and TGFβ antagonism elicits MHP formation by dynamically regulating interactions between apical (PAR complex) and basolateral (LGL) polarity proteins. TGFβ and BMP-activated receptor (r)-SMADs [phosphorylated SMAD2 or SMAD3 (pSMAD2,3), or phosphorylated SMAD1, SMAD5 or SMAD8 (pSMAD1,5,8)] undergo cell-cycle-dependent modulations and nucleo-cytosolic shuttling along the apicobasal axis of the neural plate. Non-canonical TGFβ and BMP activity in the cytosol determines whether pSMAD2,3 or pSMAD1,5,8 associates with the tight junction (PAR complex) or with LGL, and whether cell shape changes can occur at the MHP. Thus, the interactions of BMP and TGFβ with polarity proteins dynamically modulate MHP formation by regulating r-SMAD competition for tight junctions and r-SMAD sequestration by LGL.
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.