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results demonstrate the mechanism for the maintenance of the undifferentiated state of embryonic stem cells via the inhibition of the FGF4-PKCzeta-MEK-ERK1/2 pathway by O-GlcNAcylation on PKCzeta.
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The correlation in expression of FGF4 with specific stages of tooth morphogenesis support its regulatory function.
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We demonstrate with genetic evidence that the Wnt5a gradient acts as a global cue that is instructive in establishing planar cell polarity (PCP) in the limb mesenchyme, and that Wnt5a also plays a permissive role to allow Fgf4 and Fgf8 signaling to orient PCP.
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Klf5 suppresses Fgf4-Fgfr-ERK signalling, thus preventing precocious activation of the primitive endoderm specification programme
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the paternal genome facilitates the proliferation of trophoblast cells without FGF4 signaling
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There was intense Fgf4 expression observed in the PEK of the cap-stage tooth germ at E14. At E15, Fgf4 became sparse in the epithelium except for the PEK. Fgf4 was exclusively expressed in the apical end of the labial epithelium during E16-18
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With efficient chimera-forming capability using a medium containing fibroblast growth factor (FGF)-4.
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Taken together, our results demonstrated that mating behaviours influenced embryonic development in vitro by decreasing FGF4 expression.
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the amount of FGF4 is limited and regulates PE/EPI proportions in the mouse embryo.
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The role of Fgf4 in response to apoptosis and genotoxic stress is discussed.
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FGF4 is required for lineage restriction and salt-and-pepper distribution of primitive endoderm factors but not their initial expression in the mouse
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FGF4 is required to maintain a population of progenitor cells in the epiblast that generates mesoderm and contributes to the stem cell population that is incorporated in the tailbud and required for axial elongation of the mouse embryo after gastrulation.
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This study uncovers an important role of HDAC1 and histone modifications in the repression of Fgf4 and perhaps other pluripotency genes during embryonic stem cell differentiation.
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study provides genetic evidence that FGFs are the wavefront signal and identifies the data show that FGF action maintains WNT signaling, and that both signaling pathways are required in parallel to maintain PSM progenitor tissue
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Cells ceased proliferation and differentiated when FGF4, heparin, and rat embryonic fibroblasts conditioned medium were removed.
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KDM7A is a dual-specificity histone demethylase that regulates neural differentiation through FGF4.
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Trophoblast stem cell FRS2alpha mediates activation of the ERK pathway to enhance Cdx2 expression in response to FGF4. Cdx2 in turn binds to an FGF4-responsive enhancer element of the promoter region of Bmp4, leading to production and secretion of Bmp4.
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FGF4 and FGF8 regulate cell number in the nascent limb bud and are required for survival of cells located far from the AER
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p300 associates physically with and can mediate the action of the distal enhancer of the FGF-4 gene
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Fgf4 is expressed in early inner ear development.
