ArticleDevelopmental biology2015
Tak1, Smad4 and Trim33 redundantly mediate TGF-β3 signaling during palate development.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 36 citations in OpenAlex.
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- Periderm Fate during Palatogenesis: TGF-β and Periderm Dedifferentiation.Journal of dental research · 2023Article
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- A unique form of collective epithelial migration is crucial for tissue fusion in the secondary palate and can overcome loss of epithelial apoptosis.Development (Cambridge, England) · 2022Article
- The Association Between Runx Signaling and Craniofacial Development and Disease.Current osteoporosis reports · 2022Review
- FACEts of mechanical regulation in the morphogenesis of craniofacial structures.International journal of oral science · 2021Review
- Genetics and signaling mechanisms of orofacial clefts.Birth defects research · 2020Review
- Transcriptional analysis of cleft palate in TGFβ3 mutant mice.Scientific reports · 2020Article
- Regeneration of Damaged Tendon-Bone Junctions (Entheses)-TAK1 as a Potential Node Factor.International journal of molecular sciences · 2020Review
- Observation of the Epithelial Cell Behavior in the Nasal Septum During Primary Palate Closure in Mice.Frontiers in physiology · 2020Article
- Pharmacological inhibition of TAK1, with the selective inhibitor takinib, alleviates clinical manifestation of arthritis in CIA mice.Arthritis research & therapy · 2019Article
- Shox2 regulates osteogenic differentiation and pattern formation during hard palate development in mice.The Journal of biological chemistry · 2019Article
- Anterior cleft palate due to Cbfb deficiency and its rescue by folic acid.Disease models & mechanisms · 2019Article
- Trim33 is required for appropriate development of pre-cardiogenic mesoderm.Developmental biology · 2019Article
- TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion.International journal of molecular sciences · 2018Review
- Reevaluation of Pluripotent Cytokine TGF-β3 in Immunity.International journal of molecular sciences · 2018Review
- Runx1-Stat3-Tgfb3 signaling network regulating the anterior palatal development.Scientific reports · 2018Article
- Gene datasets associated with mouse cleft palate.Data in brief · 2018Article
- TGF-β Family Signaling in Mesenchymal Differentiation.Cold Spring Harbor perspectives in biology · 2018Review
- TGF-β Family Signaling in Epithelial Differentiation and Epithelial-Mesenchymal Transition.Cold Spring Harbor perspectives in biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Transforming growth factor-beta3 (TGF-β3) plays a critical role in palatal epithelial cells by inducing palatal epithelial fusion, failure of which results in cleft palate, one of the most common birth defects in humans. Recent studies have shown that Smad-dependent and Smad-independent pathways work redundantly to transduce TGF-β3 signaling in palatal epithelial cells. However, detailed mechanisms by which this signaling is mediated still remain to be elucidated. Here we show that TGF-β activated kinase-1 (Tak1) and Smad4 interact genetically in palatal epithelial fusion. While simultaneous abrogation of both Tak1 and Smad4 in palatal epithelial cells resulted in characteristic defects in the anterior and posterior secondary palate, these phenotypes were less severe than those seen in the corresponding Tgfb3 mutants. Moreover, our results demonstrate that Trim33, a novel chromatin reader and regulator of TGF-β signaling, cooperates with Smad4 during palatogenesis. Unlike the epithelium-specific Smad4 mutants, epithelium-specific Tak1:Smad4- and Trim33:Smad4-double mutants display reduced expression of Mmp13 in palatal medial edge epithelial cells, suggesting that both of these redundant mechanisms are required for appropriate TGF-β signal transduction. Moreover, we show that inactivation of Tak1 in Trim33:Smad4 double conditional knockouts leads to the palatal phenotypes which are identical to those seen in epithelium-specific Tgfb3 mutants. To conclude, our data reveal added complexity in TGF-β signaling during palatogenesis and demonstrate that functionally redundant pathways involving Smad4, Tak1 and Trim33 regulate palatal epithelial fusion.
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.