ArticleDisease models & mechanisms2022
Ras signaling and RREB1 are required for the dissociation of medial edge epithelial cells in murine palatogenesis.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Pan-Ras-In-1 triggers cell wall lysis to eradicateiScience · 2026Article
- A Novel Loss-of-Function Variant inGenes · 2026Article
- The roles of JAK2/STAT3 signaling in fusion of the secondary palate.Disease models & mechanisms · 2023Article
- Impactful in disease research: a DMM year in review.Disease models & mechanisms · 2023Article
- Effects of Dietary Koumine on Growth Performance, Intestinal Morphology, Microbiota, and Intestinal Transcriptional Responses ofInternational journal of molecular sciences · 2022Article
- Understanding and drugging RAS: 40 years to break the tip of the iceberg.Disease models & mechanisms · 2022Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
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Abstract
Cleft palate is one of the major congenital craniofacial birth defects. The etiology underlying the pathogenesis of cleft palate has yet to be fully elucidated. Dissociation of the medial edge epithelium (MEE) at the contacting region of palatal shelves and subsequent migration or apoptosis of MEE cells is required for proper MEE removal. Ras-responsive element-binding protein 1 (RREB1), a RAS transcriptional effector, has recently been shown to play a crucial role in developmental epithelial-mesenchymal transition (EMT), in which loss of epithelial characteristics is an initial step, during mid-gastrulation of embryonic development. Interestingly, the involvement of RREB1 in cleft palate has been indicated in humans. Here, we demonstrated that pan-Ras inhibitor prevents the dissociation of MEE during murine palatal fusion. Rreb1 is expressed in the palatal epithelium during palatal fusion, and knockdown of Rreb1 in palatal organ culture resulted in palatal fusion defects by inhibiting the dissociation of MEE cells. Our present findings provide evidence that RREB1-mediated Ras signaling is required during palatal fusion. Aberrant RREB1-mediated Ras signaling might be involved in the pathogenesis of cleft palate.
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