ArticleJournal of cellular physiology2011
Mechanisms of transforming growth factor β induced cell cycle arrest in palate development.
Article in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Risk Prediction of Colon Cancer Metastasis and Bioinformatics Analysis of Aspirin Treatment.International journal of genomics · 2025Article
- Introduction of miR-3613-3p as a regulator of transforming growth factor-β (TGF-β) signaling pathway in colorectal cancer.Molecular biology reports · 2024Article
- Interleukin-22 Inhibits Apoptosis of Gingival Epithelial Cells Through TGF-β Signaling Pathway During Periodontitis.Inflammation · 2023Article
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- Integrin-linked kinase tunes cell-cell and cell-matrix adhesions to regulate the switch between apoptosis and EMT downstream of TGFβ1.Molecular biology of the cell · 2021Article
- Evaluation of TGF-β1 and EGFR in Cleft Affected Lip Mucosa.Acta medica Lituanic · 2021Review
- Identification of New miRNA-mRNA Networks in the Development of Non-syndromic Cleft Lip With or Without Cleft Palate.Frontiers in cell and developmental biology · 2021Article
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- Integrated analysis identifying long non-coding RNAs (lncRNAs) for competing endogenous RNAs (ceRNAs) network-regulated palatal shelf fusion in the development of mouse cleft palate.Annals of translational medicine · 2019Article
- Investigating epithelial-to-mesenchymal transition with integrated computational and experimental approaches.Physical biology · 2019Review
- Divide or Conquer: Cell Cycle Regulation of Invasive Behavior.Trends in cell biology · 2017Review
- Transforming growth factor-β1 activates ΔNp63/c-Myc to promote oral squamous cell carcinoma.Oral surgery, oral medicine, oral pathology and oral radiology · 2016Article
- Expression of transforming growth factor β1 promotes cholangiocarcinoma development and progression.Cancer letters · 2016Article
- Ephrin reverse signaling mediates palatal fusion and epithelial-to-mesenchymal transition independently of Tgfß3.Journal of cellular physiology · 2015Article
- Role of Bruton's tyrosine kinase inhibitors in HIV-1-infected cells.Journal of neurovirology · 2015Article
- Downregulation of HO-1 promoted apoptosis induced by decitabine via increasing p15INK4B promoter demethylation in myelodysplastic syndrome.Gene therapy · 2015Article
- Age-specific functional epigenetic changes in p21 and p16 in injury-activated satellite cells.Stem cells (Dayton, Ohio) · 2015Article
- Tak1, Smad4 and Trim33 redundantly mediate TGF-β3 signaling during palate development.Developmental biology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Immaculate and complete palatal seam disintegration, which takes place at the last phase of palate development, is essential for normal palate development. And in absence of palatal midline epithelial seam (MES) disintegration, cleft palate may arise. It has been established that transforming growth factor (TGF) β induces both epithelial mesenchymal transition (EMT) and/or apoptosis during MES disintegration. It is likely that MES might cease cell cycle to facilitate cellular changes prior to undergoing transformation or apoptosis, which has never been studied before. This study was designed to explore whether TGFβ, which is crucial for palatal MES disintegration, is capable of inducing cell cycle arrest. We studied the effects of TGFβ1 and TGFβ3, potent negative regulators of the cell cycle, on p15ink4b activity in MES cells. We surprisingly found that TGFβ1, but not TGFβ3, plays a major role in activation of the p15ink4b gene. In contrast, following successful cell cycle arrest by TGFβ1, it is TGFβ3 but not TGFβ1 that causes later cellular morphogenesis, such as EMT and apoptosis. Since TGFβ signaling activates Smads, we analyzed the roles of three Smad binding elements (SBEs) on the p15ink4b mouse promoter by site specific mutagenesis and found that these binding sites are functional. The ChIP assay demonstrated that TGFβ1, not TGFβ3, promotes Smad4 binding to two 5' terminal SBEs but not the 3' terminal site. Thus, TGFβ1 and TGFβ3 play separate yet complimentary roles in achieving cell cycle arrest and EMT/apoptosis and cell cycle arrest is a prerequisite for later cellular changes.
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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.