Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent - Wikidata - awgldk - TriplyDB

Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent

Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent

http://www.wikidata.org/entity/Q36780832

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A Genetic-Pathophysiological Framework for Craniosynostosis Fibroblast growth factor signaling in skeletal development and disease Developmental and Evolutionary Significance of the Zygomatic Bone Tissue-nonspecific alkaline phosphatase deficiency causes abnormal craniofacial bone development in the Alpl(-/-) mouse model of infantile hypophosphatasia The effects of tissue-non-specific alkaline phosphatase gene therapy on craniosynostosis and craniofacial morphology in the FGFR2C342Y/+ mouse model of Crouzon craniosynostosis.Mechanical properties of calvarial bones in a mouse model for craniosynostosis.Enzyme replacement for craniofacial skeletal defects and craniosynostosis in murine hypophosphatasia.Periodontal Defects in the A116T Knock-in Murine Model of Odontohypophosphatasia.Tissue Nonspecific Alkaline Phosphatase (TNAP) Regulates Cranial Base Growth and Synchondrosis Maturation.Bone mineralization-dependent craniosynostosis and craniofacial shape abnormalities in the mouse model of infantile hypophosphatasia.FGFR2c-mediated ERK-MAPK activity regulates coronal suture development.Postnatal Craniofacial Skeletal Development of Female C57BL/6NCrl Mice.Craniosynostosis-associated Fgfr2(C342Y) mutant bone marrow stromal cells exhibit cell autonomous abnormalities in osteoblast differentiation and bone formation.Predicting calvarial growth in normal and craniosynostotic mice using a computational approach.Osteogenesis of Crouzon-Mutated Cells in an Experimental Model.

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Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent

http://www.wikidata.org/entity/Q36780832

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2013 nî lūn-bûn

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Further analysis of the Crouzo ...... ion are cranial bone-dependent

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Estee Wang

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Hwa Kyung Nam

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Nan E Hatch

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P2860

Mutations in the fibroblast growth factor receptor 2 gene cause Crouzon syndrome

Drug export activity of the human canalicular multispecific organic anion transporter in polarized kidney MDCK cells expressing cMOAT (MRP2) cDNA

Growth of the normal skull vault and its alteration in craniosynostosis: insights from human genetics and experimental studies

Priorities for public health research on craniosynostosis: summary and recommendations from a Centers for Disease Control and Prevention-sponsored meeting

Mutations in FGFR1 and FGFR2 cause familial and sporadic Pfeiffer syndrome

Early onset of craniosynostosis in an Apert mouse model reveals critical features of this pathology

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

Activation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2(+P253R) mice.

Differential FGF ligands and FGF receptors expression pattern in frontal and parietal calvarial bones

Activation of FGF signaling mediates proliferative and osteogenic differences between neural crest derived frontal and mesoderm parietal derived bone.

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