ArticleCellular signalling2012
Endocardial cell epithelial-mesenchymal transformation requires Type III TGFβ receptor interaction with GIPC.
Article in Cellular signalling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Exploring TGFBR3 in disease pathogenesis: Mechanisms, clinical implications, and pharmacological modulation.Journal of pharmaceutical analysis · 2026Review
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- Biallelic loss-of-function variants in PLD1 cause congenital right-sided cardiac valve defects and neonatal cardiomyopathy.The Journal of clinical investigation · 2021Article
- Endothelial to Mesenchymal Transition in the Cardiogenesis and Cardiovascular Diseases.Current cardiology reviews · 2020Review
- A familial congenital heart disease with a possible multigenic origin involving a mutation in BMPR1A.Scientific reports · 2019Article
- Hemodynamics in Cardiac Development.Journal of cardiovascular development and disease · 2018Article
- Dually modified transmembrane proteoglycans in development and disease.Cytokine & growth factor reviews · 2018Review
- DNA Methylation Profiling Reveals the Change of Inflammation-AssociatedFrontiers in aging neuroscience · 2018Article
- A Selective Transforming Growth Factor-β Ligand Trap Attenuates Pulmonary Hypertension.American journal of respiratory and critical care medicine · 2016Article
- Common pathways regulate Type III TGFβ receptor-dependent cell invasion in epicardial and endocardial cells.Cellular signalling · 2016Article
- Article
- Association of TGFBR2 rs6785358 Polymorphism with Increased Risk of Congenital Ventricular Septal Defect in a Chinese Population.Pediatric cardiology · 2015Article
- Simvastatin alleviates cardiac fibrosis induced by infarction via up-regulation of TGF-β receptor III expression.British journal of pharmacology · 2015Article
- Type III TGFβ receptor and Src direct hyaluronan-mediated invasive cell motility.Cellular signalling · 2015Article
- Reprogramming during epithelial to mesenchymal transition under the control of TGFβ.Cell adhesion & migration · 2015Review
- Myocardial contraction and hyaluronic acid mechanotransduction in epithelial-to-mesenchymal transformation of endocardial cells.Biomaterials · 2014Article
- The chick embryo as an expanding experimental model for cancer and cardiovascular research.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Review
- Induction of transforming growth factor beta receptors following focal ischemia in the rat brain.PloS one · 2014Article
- Functional proteomics, human genetics and cancer biology of GIPC family members.Experimental & molecular medicine · 2013Review
- Atrioventricular valve development: new perspectives on an old theme.Differentiation; research in biological diversity · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
An early event in heart valve formation is the epithelial-mesenchymal transformation (EMT) of a subpopulation of endothelial cells in specific regions of the heart tube, the endocardial cushions. The Type III TGFβ receptor (TGFβR3) is required for TGFβ2- or BMP-2-stimulated EMT in atrioventricular endocardial cushion (AVC) explants in vitro but the mediators downstream of TGFβR3 are not well described. Using AVC and ventricular explants as an in vitro assay, we found an absolute requirement for specific TGFβR3 cytoplasmic residues, GAIP-interacting protein, C terminus (GIPC), and specific Activin Receptor-Like Kinases (ALK)s for TGFβR3-mediated EMT when stimulated by TGFβ2 or BMP-2. The introduction of TGFβR3 into nontransforming ventricular endocardial cells, followed by the addition of either TGFβ2 or BMP-2, results in EMT. TGFβR3 lacking the entire cytoplasmic domain, or only the 3C-terminal amino acids that are required to bind GIPC, fails to support EMT in response to TGFβ2 or BMP-2. Overexpression of GIPC in AVC endocardial cells enhanced EMT while siRNA-mediated silencing of GIPC in ventricular cells overexpressing TGFβR3 significantly inhibited EMT. Targeting of specific ALKs by siRNA revealed that TGFβR3-mediated EMT requires ALK2 and ALK3, in addition to ALK5, but not ALK4 or ALK6. Taken together, these data identify GIPC, ALK2, ALK3, and ALK5 as signaling components required for TGFβR3-mediated endothelial cell EMT.
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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.