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During embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs.
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Fgfr2 mediated FGF signaling in palate mesenchymal cells is functionally required for palate development at various stages including a possible role in shelf initiation out of the maxillary process on E11.5.
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gain-of-function mutation in FGFR2 exerts a Wnt/beta-catenin-dependent anabolic effect on trabecular bone by promoting bone formation.
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small interfering RNA knockdown of FGFR2 suppressed PI3K/Akt pathway activation by FGF10 and abolished its anti-apoptotic and neurite repair effects in vitro.
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Testis determination involves FGFR2c-mediated repression of both the WNT4- and FOXL2-driven ovarian-determining pathways.
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The results of this study showed that GF22KO mice display longer duration of floating and decreased latency to float in the forced swim test, increased immobility in the tail suspension test, and decreased preference for sucrose in the sucrose preference test, which are all suggestive of a depressive-like phenotype.
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the localization of FGF9 and its receptors at different embryonic and postnatal stages in mice testes, was examined.
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FGFR2 signalling correlates with maintenance of expression of a key transcription factor for basal cell self-renewal and differentiation: SOX2.
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Fgfr2 is seen within submucosal glandular epithelial cells. The medial nasal glands were missing in Fgfr2b mutants.
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It is well accepted that myelin is a biologically active membrane in active communication with the axons. However, the axonal signals, the receptors on myelin, and the integration of intracellular signaling pathways emanating downstream from these receptors that drive the growth of the myelin sheath remain poorly understood in the CNS. This study brings up the intriguing possibility that FGF receptor 2, in the oligodendr
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data suggest that FGF2 levels are critically related to anxiety behavior and hypothalamic pituitary- adrenal axis activity, likely through modulation of hippocampal glucocorticoid receptor expression, an effect that is likely receptor mediated, albeit not by FGFR1, FGFR2, and FGFR3.
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Results show that Fgfr2 regulates both the formation and resolution of tetrads and rosettes in the mouse embryo, possibly in part by spatially restricting atypical protein kinase C, a negative regulator of non-muscle myosin IIB.
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FGFR2c signaling regulates branching morphogenesis through the activation of FGFR2b signaling via increased FGF10 autocrine. These results provide new insight into the mechanisms by which crosstalk between FGFR2b and FGFR2c results in efficient branching morphogenesis.
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Fgfr2 is critical for bladder mesenchyme patterning by virtue of its role in modulation of hedgehog signaling
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Ectopic expression of Fgfr2c was detected within the affected sutures of Bcl11b(-/-) mice. Ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice.
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Calvarial osteoblasts from Fgfr2c gain-of-function mice had enhanced osteoblastic function and maturation with concomitant increase in ERK-MAPK activation. In vitro inhibition with U0126 mitigated ERK protein activation levels and reduced alkaline phosphatase activity. FGFR2c-mediated ERK-MAPK signaling is a key mediator of craniofacial growth and coronal suture development.
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these data suggest that tropism of influenza Virus to distal lung stem cell niches represents an important factor of pathogenicity and highlight impaired Fgfr2b signaling as underlying mechanism
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Fgfr1 and Fgfr2 in the palatal and mandibular mesenchyme have roles in regulating shelf medial wall protrusion and growth of the mandible to coordinate the craniofacial tissue movements that are required for palatal shelf elevation
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Data demonstrate an essential role for FGFR1 and FGFR2 in endothelial cells for cardiac functional recovery and vascular remodeling following in vivo cardiac ischemia-reperfusion injury, without affecting the cardiac hypertrophic response.
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isolated deletion of Pten failed to stimulate ectopic fiber cell differentiation, and the combined deletion of Pten and Fgfr2 failed to restore differentiation-specific Aquaporin0 and DnaseIIbeta expression in the lens fiber cells
