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mesenchymal cells of the skull are not fated to form bone, but can be forced into a chondrogenic fate through the manipulation of FGF8 signaling.
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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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THe Fgf8-Cre reporter expression in isthmic structures in mice include 'signature' isthmic structures in mice include the trochlear nucleus, the dorsal raphe nucleus, the microcellular tegmental nuclei, the pedunculotegmental nucleus, the vermis of the cerebellum, rostral parts of the parabrachial complex and locus coeruleus, and the caudal parts of the substantia nigra and VTA.
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Results indicate that perinatal fibroblast growth factor 8 (FGF8) signaling is important for the timing of the onset of anterior-dorsal glial fibrillary acidic protein expression in midline glial cells suggesting that FGF8 function regulates midline GFAP-IR glial cell development, which when disrupted by Fgf8 deficiency prevents the formation of the corpus callosum.
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The FBLN1/FGF8 interaction may also be involved in the survival of neural crest cell population during development.
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These results indicate that the modulatory effects of SHH on BALB/c mouse metanephric explant cultures may involve the regulation of Fgf8 expression but not Fgf10 expression, which provides evidence for the functional role of Fgf proteins in renal morphogenesis.
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FGF-8 was revealed to suppress BMP-induced osteoblast differentiation through the ERK pathway and the effects were enhanced by TNF-alpha.
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Fgf8 expression is required for the continued postnatal development/maturation of the Vasopressin and CRH neurons in the Paraventricular nucleus.
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Deregulated FGF8 and Otx2/Gbx2 gene expression underlies cerebellar vermis hypoplasia in mouse model of CHARGE syndrome.
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Cre fate mapping in Fgf8 mutant embryos revealed novel functions of this gene in rostral patterning center progenitor development. Disruption resulted in aberrant progenitor number and distribution in the rostral telencephalon.
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Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage
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Results show that DLX5, p63, Pin1 and FGF8 participate to the same time- and location-restricted regulatory loop essential for apical ectodermal ridge stratification, hence for normal patterning and skeletal morphogenesis of the limb buds.
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This study demonistrated that Fgf8- and Fgfr1/Fgf8-deficient mice diplay increased anxiety-like behavior and reductions in specific populations of serotonergic neurons in the brain.
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Scube3 may be a critical upstream regulator of fast fiber myogenesis by modulating fgf8 signaling during zebrafish embryogenesis
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Retinoic acid directly represses Fgf8 through a retinoic acid response element-mediated mechanism that promotes repressive chromatin
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Together our data demonstrates that Foxc1 - Fgf8 signaling regulates mammalian jaw patterning and provides a mechanistic basis for the pathogenesis of syngnathia
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Data indicate that Foxi3 mutants succumb to apoptosis from embryonic day 9.75 onwards, and this cell death correlates with a delay in expression of Fgf8 in branchial arch ectoderm.
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FGF8 is not sufficient to induce ectodermal progenitors of the olfactory pit to acquire neural fate. altered neurogenesis and lack of GnRH neuron specification after reduced Fgf8 expression reflected dysgenesis of the nasal region.
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regulation of higher order chromatin organisation during differentiation in the embryo can be uncoupled from the machinery that promotes transcription and, for the first time, identify FGF as an extrinsic signal that can direct chromatin compaction
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In Fuz mutants, the phenotype stems from dysregulated Gli processing, which in turn results in excessive craniofacial Fgf8 gene expression.
