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A Sprouty4 reporter to monitor FGF/ERK signaling activity in ESCs and mice.
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Irf6 and RTK signaling interact in regulating periderm differentiation and function, as well as provide a rationale to screen for epistatic interactions between variants in IRF6 and RTK signaling pathway genes in human orofacial clefting populations.
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In the present study, it is demonstrated that Spry2 and -4 participate in KA induced neurodegeneration possibly through inhibition of ERK signaling.
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Autoregulatory loop between TGF-beta1/miR-411-5p/SPRY4 and p38 MAPK pathway in rhabdomyosarcoma modulates proliferation and differentiation.
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in embryos with lower Spry2;Spry4 gene dosages, we observed a non-fusion of original R2 and M1 Shh signaling domains with consequent formation of a supernumerary tooth primordium from the isolated R2 bud
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We demonstrate that in spry4-/- mice inflammatory responses, such TNFalpha secretion and macrophage/neutrophil invasion into the lesion site are reduced. In addition, astrocytic gliosis is attenuated and neuronal survival is increased.
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SPRY4 is a tumor suppressor at 5q whose disruption contributes to a lethal acute myeloid leukemia subtype.
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In vivo analysis revealed that Spry4 regulated integrin beta3 levels in murine embryos and yolk sacs.
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We propose that Sprouty genes(Spry2 and Spry4) were implicated during evolution in reduction of the cheek teeth in Muridae, and their deletion can reveal ancestral stages of murine dental evolution.
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ISG15 mRNA expression and IFN-dependent antiviral responses are enhanced in Spry1,2,4 triple knock-out mouse embryonic fibroblasts, consistent with negative feedback regulatory roles for Spry proteins in IFN-mediated signaling.
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our results imply that Sprouty2 and -4 are downregulated in the hippocampus during postnatal brain development and that they can act as regulators of developmental axon growth.
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Interestingly, changes in sprouty gene dosage led to a graded change in incisor number, with progressive decreases in sprouty dosage leading to increasing numbers of teeth.
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Spry4 and Tpbg/5T4 were detected in Kit-immunoreactive cells only in Kit(K641E), but not in Kit(WT/WT) animals.
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Spry4, an intracellular FGF receptor antagonist, was expressed in epithelial cells of the fetal lung under control of a doxycycline-inducible system.
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suggest both redundant and non-redundant functions for Sprouty2 and Sprouty4 on embryonic development and FGF signaling
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Transgenic expression of murine Spry4 during beta-cell carcinogenesis does not significantly affect tumor outgrowth and progression to tumor malignancy.
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These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases.
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Periodic expression of Sprouty4 is controlled by the Notch segmentation clock and may work as a mediator that links the temporal periodicity of clock gene oscillations with the spatial periodicity of boundary formation.
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Sprouty4 deficiency potentiates Ras-independent angiogenic signals and tumor growth.