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After the formation of the epithelial bud, the expressions of Fgf10 and Fgf18, as well as that of Fgf3, are found; besides, Fgfr2IIIc expression appears .
Comparative PCR array analysis has shown an increased statistical significance (14-fold) in the Fgf3 expression levels between E13.0 and E15.0 .
FGF expression patterns suggest that the binding of FGF3 and FGF10 to FGFR2IIIb activate FGF signaling from the epithelium at the stages of invagination and tooth bud [64, 65].
Given that FGF3 and FGF10 bind to FGFR2IIIb, it is important for these FGFs to be involved in the transitional process to the tooth bud [77, 78].
With exogenous FGF4, Fgf3 expression is rapidly induced in mesenchyme and the defect in [Lef1.sup.-/-] tooth germs is fully rescued .
Mansour, "Fgf3 and Fgf10 are required for mouse otic placode induction," Development, vol.
FGF3 in the floor plate directs notochord convergent extension in the Ciona tadpole.
FGF3 and FGF10 have some form of functional redundancy, as Fgf3-/- or Fgf10-/- mice develop teeth normally, but mice that lack the FgfR2b receptor (the receptor for Fgf3 and Fgf10) exhibit teeth that arrest at the bud stage [Zhang et al., 2005].
Cbfa1/Runx2 protein is a critical transcriptional regulator of osteoblast differentiation that is down-regulated by Msx1 most likely via FGF3 [Zhang et al., 2005].
Additionally, Fgf4 regulates factors that limit ossification (Fgf3) and other factors that control osteoblast differentiation and function (Runx2).
If Msx1 or Pax9 are not expressed, the mesenchyme will not be activated to release Bmp4, which in turn causes Lef1, Dlx2, Plx2, Ptc, and Fgf3, to not be expressed, and the tooth bud will not develop to the cap stage [Zhao et al., 2000; Matalova et al., 2008; De Coster et al., 2009].
Down-regulation of Msx1 causes a decrease in Fgf8; Fgf8 does not signal Fgf3; Fgf3 does not signal Syndecan-1; the absence of Syndecan-1 causes cessation of tooth development during the cap stage [Zhao et al., 2000].
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- FGF-inducible kinase