In vivo modulation of FGF biological activity alters cranial suture fate - Wikidata - wikimedia - TriplyDB

In vivo modulation of FGF biological activity alters cranial suture fate

In vivo modulation of FGF biological activity alters cranial suture fate

http://www.wikidata.org/entity/Q35746278

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Mechanical influences on suture development and patency Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis Craniosynostosis in Twist heterozygous mice: a model for Saethre-Chotzen syndrome High-dose retinoic acid modulates rat calvarial osteoblast biology.Distribution of fibroblast growth factors (FGFR-1 and -3) and platelet-derived growth factor receptors (PDGFR) in the rat mandibular condyle during growth.Estrogen/estrogen receptor alpha signaling in mouse posterofrontal cranial suture fusion.Paracrine interaction between adipose-derived stromal cells and cranial suture-derived mesenchymal cells.The BMP antagonist noggin regulates cranial suture fusion.Effects of thyroxine exposure on osteogenesis in mouse calvarial pre-osteoblasts.New therapeutic targets in rare genetic skeletal diseases.Augmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice.Differential effects of TGF-beta1 and TGF-beta3 on chondrogenesis in posterofrontal cranial suture-derived mesenchymal cells in vitro.The role of vertebrate models in understanding craniosynostosis.Craniofacial surgery, from past pioneers to future promise.Models of cranial suture biology.Craniosynostosis: molecular pathways and future pharmacologic therapy.A soluble form of fibroblast growth factor receptor 2 (FGFR2) with S252W mutation acts as an efficient inhibitor for the enhanced osteoblastic differentiation caused by FGFR2 activation in Apert syndrome.Medical treatment of craniosynostosis: recombinant Noggin inhibits coronal suture closure in the rat craniosynostosis model.BCL11B regulates sutural patency in the mouse craniofacial skeleton.Bone morphogenetic protein is required for fibroblast growth factor 2-dependent later-stage osteoblastic differentiation in cranial suture cells.Cranial bone defect healing is accelerated by mesenchymal stem cells induced by coadministration of bone morphogenetic protein-2 and basic fibroblast growth factor.Noggin inhibits postoperative resynostosis in craniosynostotic rabbits.Rapamycin rescues BMP mediated midline craniosynostosis phenotype through reduction of mTOR signaling in a mouse model Craniosynostosis, psychomotor retardation, and facial dysmorphic features in a Spanish patient with a 4q27q28.3 deletion Relaxin does not rescue coronal suture fusion in craniosynostotic rabbits Genetic basis of potential therapeutic strategies for craniosynostosis

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P2860

In vivo modulation of FGF biological activity alters cranial suture fate

http://www.wikidata.org/entity/Q35746278

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2001年論文

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In vivo modulation of FGF biological activity alters cranial suture fate

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In vivo modulation of FGF biological activity alters cranial suture fate

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In vivo modulation of FGF biological activity alters cranial suture fate

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In vivo modulation of FGF biological activity alters cranial suture fate

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In vivo modulation of FGF biological activity alters cranial suture fate

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S0002-9440(10)63987-9

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The American Journal of Pathology

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In vivo modulation of FGF biological activity alters cranial suture fate

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B J Mehrara

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F E Crisera

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H Ueno

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J A Greenwald

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M T Longaker

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P J Fagenholz

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S M Warren

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P2860

FGF-, BMP- and Shh-mediated signalling pathways in the regulation of cranial suture morphogenesis and calvarial bone development

Constitutive receptor activation by Crouzon syndrome mutations in fibroblast growth factor receptor (FGFR)2 and FGFR2/Neu chimeras

Ligand-independent activation of fibroblast growth factor receptors by point mutations in the extracellular, transmembrane, and kinase domains

Increased calvaria cell differentiation and bone matrix formation induced by fibroblast growth factor receptor 2 mutations in Apert syndrome

Activating mutations in the extracellular domain of the fibroblast growth factor receptor 2 function by disruption of the disulfide bond in the third immunoglobulin-like domain

Apert syndrome mutations in fibroblast growth factor receptor 2 exhibit increased affinity for FGF ligand

Tissue interactions with underlying dura mater inhibit osseous obliteration of developing cranial sutures.

Cranial sutures require tissue interactions with dura mater to resist osseous obliteration in vitro.

Dura mater maintains rat cranial sutures in vitro by regulating suture cell proliferation and collagen production.

Molecular genetic advances in understanding craniosynostosis.

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