Increased osteoblast apoptosis in apert craniosynostosis: role of protein kinase C and interleukin-1.
about
Intracellular retention, degradation, and signaling of glycosylation-deficient FGFR2 and craniosynostosis syndrome-associated FGFR2C278FFibroblast growth factor signaling in skeletal development and diseaseOverexpression of Nell-1, a craniosynostosis-associated gene, induces apoptosis in osteoblasts during craniofacial developmentActivation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2(+P253R) mice.Role of N-cadherin in bone formation.Comprehensive functional annotation of seventy-one breast cancer risk Loci.Inhibited Wnt signaling causes age-dependent abnormalities in the bone matrix mineralization in the Apert syndrome FGFR2(S252W/+) miceAdvanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways.FGF and FGFR signaling in chondrodysplasias and craniosynostosis.Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependentAugmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice.A Ser252Trp mutation in fibroblast growth factor receptor 2 (FGFR2) mimicking human Apert syndrome reveals an essential role for FGF signaling in the regulation of endochondral bone formation.FGF/FGFR signaling in bone formation: progress and perspectives.Role of FGFs/FGFRs in skeletal development and bone regeneration.E3 ubiquitin ligase-mediated regulation of bone formation and tumorigenesis.The molecular and cellular basis of Apert syndrome.Potential role of PC-1 expression and pyrophosphate elaboration in the molecular etiology of the FGFR-associated craniosynostosis syndromes.Functional characterization of a novel FGFR2 mutation, E731K, in craniosynostosis.Fibroblast growth factor receptor 2 promotes osteogenic differentiation in mesenchymal cells via ERK1/2 and protein kinase C signaling.Sprouty genes are expressed in osteoblasts and inhibit fibroblast growth factor-mediated osteoblast responses.FGFR2 mutation confers a less drastic gain of function in mesenchymal stem cells than in fibroblasts.Bone morphogenetic protein-2 promotes osteoblast apoptosis through a Smad-independent, protein kinase C-dependent signaling pathway.Delivery of Transforming Growth Factor-β3 Plasmid in a Collagen Gel Inhibits Cranial Suture Fusion in Rats.Nell-1 induces acrania-like cranioskeletal deformities during mouse embryonic development.The Fgfr2(S252W/+) mutation in mice retards mandible formation and reduces bone mass as in human Apert syndrome.Genetic basis of potential therapeutic strategies for craniosynostosisPathology teach and tell: acrocephalosyndactyly type I (Apert syndrome)Research advances in Apert syndrome
P2860
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P2860
Increased osteoblast apoptosis in apert craniosynostosis: role of protein kinase C and interleukin-1.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
2001年论文
@zh
2001年论文
@zh-cn
name
Increased osteoblast apoptosis ...... in kinase C and interleukin-1.
@en
type
label
Increased osteoblast apoptosis ...... in kinase C and interleukin-1.
@en
prefLabel
Increased osteoblast apoptosis ...... in kinase C and interleukin-1.
@en
P2093
P2860
P1476
Increased osteoblast apoptosis ...... ein kinase C and interleukin-1
@en
P2093
D Modrowski
J Lemonnier
O Fromigué
P Delannoy
P2860
P304
P356
10.1016/S0002-9440(10)64139-9
P407
P577
2001-05-01T00:00:00Z