Brief noteDifferential expression of genes encoding TGFs β1, β2, and β3 during murine palate formation
References (21)
- et al.
Migratory behaviour of cardiac cushion cells in a colagen-lattice culture system
Dev. Biol
(1982) - et al.
The murine transforming growth factor-beta precursor
J. Biol. Chem
(1986) - et al.
Medial edge epithelium transforms to mesenchyme after embryonic palatal shelves fuse
Dev. Biol
(1989) - et al.
Epithelial-mesenchymal cell transformation in the embryonic heart can be mediated, in part, by transforming growth factor β
Dev. Biol
(1989) - et al.
The epithelial-mesenchymal interface of the rat Müllerian duct: Loss of basement membrane integrity and ductal regression
Dev. Biol
(1982) - et al.
Retinoids and EGF alter embryonic mouse palatal epithelial and mesenchymal cell differentiation in organ culture
J. Craniofacial Genet. Dev. Biol
(1987) - et al.
Effects of hyaluronic acid on cardiac cushion cells in collagen matrix cultures
Tex. Rep. Biol. Med
(1979) Palate development: Mechanisms and malformations
Ir. J. Med. Sci
(1987)Palate development
Development
(1988)- et al.
Retinoic acid induces transforming growth factor-β2 in cultured keratinocytes and mouse epidermis
Cell Regul
(1989)
Cited by (175)
Mouse models in palate development and orofacial cleft research: Understanding the crucial role and regulation of epithelial integrity in facial and palate morphogenesis
2022, Current Topics in Developmental BiologyFoxf2 is required for secondary palate development and Tgfβ signaling in palatal shelf mesenchyme
2016, Developmental BiologyCellular and Molecular Mechanisms of Palatogenesis
2015, Current Topics in Developmental BiologyStrain-dependent effects of transforming growth factor-β1 and 2 during mouse secondary palate development
2014, Reproductive ToxicologyCitation Excerpt :TGF-β1, 2, and 3 are the three major TGF-β members that signal through TGF-β type I and type II receptors [18]. The function of TGF-β3 during palate development has been well studied [22–27]. During palate development, TGF-β3 is expressed exclusively in palate epithelium and plays an essential role in mediating palate fusion and seam degeneration, since the Tgf-β3−/− mutant embryos display cleft palate directly due to a fusion defect [26,27].
Epigenetic analysis of laser capture microdissected fetal epithelia
2013, Analytical BiochemistryCitation Excerpt :Both kits were also used to evaluate extracted levels of two mRNAs expressed in the MEE: Mmp13 and Tgfβ3 (Table 4). Mmp13 is almost exclusively localized in both epithelial and mesenchymal cells at the site of palatal fusion [54], whereas Tgfβ3 is specifically expressed in cells of the MEE during palatal fusion [55,56] as well as in the oral and nasal epithelia of palatal tissue. The RNAqueous Micro kit was considerably more efficient in extracting Mmp-13 mRNA, but not Tgfβ3 mRNA, from both scraped and LCM-procured tissue.
Intra-amniotic transient transduction of the periderm with a viral vector encoding TGFβ3<sup>-/-</sup> prevents cleft palate in Tgfβ3 <sup>-/-</sup> mouse embryos
2013, Molecular TherapyCitation Excerpt :The fusion defect is fully rescued in E14.5 Tgfβ3−/− palatal organ cultures by supplementing the culture media with rhTGFβ3.15 Consistent with its primary importance in palatal fusion, TGFβ3 expression is dramatically increased in the MEE at the time of fusion, which begins at E13 and peaks at E14/14.5.16 In humans, TGFβ3 gene variants are associated with increased risk of nonsyndromic cleft lip/palate.17,18,19,20
- 2
R.W.P. is supported by the Medical Scientist Training Program (MSTP) of the NIH, Grant T32-GM07347.