Mesodermal expression of Fgfr2S252W is necessary and sufficient to induce craniosynostosis in a mouse model of Apert syndrome.
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A Genetic-Pathophysiological Framework for CraniosynostosisReceptor tyrosine kinase signaling: regulating neural crest development one phosphate at a timeCraniofacial divergence by distinct prenatal growth patterns in Fgfr2 mutant miceMorphological comparison of the craniofacial phenotypes of mouse models expressing the Apert FGFR2 S252W mutation in neural crest- or mesoderm-derived tissues.Characterization of distinct classes of differential gene expression in osteoblast cultures from non-syndromic craniosynostosis boneThe Fibroblast Growth Factor signaling pathwayGene expression changes between patent and fused cranial sutures in a nonsyndromic craniosynostosis populationMechanical properties of calvarial bones in a mouse model for craniosynostosis.Effects of Usag-1 and Bmp7 deficiencies on murine tooth morphogenesis.Molecular mechanisms of midfacial developmental defects.Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependentFrom shape to cells: mouse models reveal mechanisms altering palate development in Apert syndromeHand in glove: brain and skull in development and dysmorphogenesis.Fibroblast growth factor (FGF) signaling in development and skeletal diseases.Signaling networks in joint development.Effects of thyroxine exposure on the Twist 1 +/- phenotype: A test of gene-environment interaction modeling for craniosynostosisCraniofacial shape variation in Twist1+/- mutant mice.Syndromic Craniosynostosis Can Define New Candidate Genes for Suture Development or Result from the Non-specifc Effects of Pleiotropic Genes: Rasopathies and Chromatinopathies as Examples.Dysregulated PDGFRα signaling alters coronal suture morphogenesis and leads to craniosynostosis through endochondral ossification.Mouse models of Apert syndrome.Developmental constraint through negative pleiotropy in the zygomatic arch.Research advances in Apert syndromeQuantification of gene expression patterns to reveal the origins of abnormal morphogenesis
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Mesodermal expression of Fgfr2S252W is necessary and sufficient to induce craniosynostosis in a mouse model of Apert syndrome.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
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name
Mesodermal expression of Fgfr2 ...... mouse model of Apert syndrome.
@en
type
label
Mesodermal expression of Fgfr2 ...... mouse model of Apert syndrome.
@en
prefLabel
Mesodermal expression of Fgfr2 ...... mouse model of Apert syndrome.
@en
P2860
P1476
Mesodermal expression of Fgfr2 ...... mouse model of Apert syndrome.
@en
P2093
Claudio Basilico
Greg Holmes
P2860
P304
P356
10.1016/J.YDBIO.2012.05.026
P407
P577
2012-06-01T00:00:00Z