Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
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Wnt signaling in cartilage development and diseases: lessons from animal studiesRole and Mechanisms of Actions of Thyroid Hormone on the Skeletal DevelopmentHistone deacetylase 7 (Hdac7) suppresses chondrocyte proliferation and β-catenin activity during endochondral ossificationGap junction communication between uterine stromal cells plays a critical role in pregnancy-associated neovascularization and embryo survival.Neurodevelopment in schizophrenia: the role of the wnt pathways.Lrp4, a novel receptor for Dickkopf 1 and sclerostin, is expressed by osteoblasts and regulates bone growth and turnover in vivo.Early articular cartilage degeneration in a developmental dislocation of the hip model results from activation of β-catenin.BMP-2 modulates beta-catenin signaling through stimulation of Lrp5 expression and inhibition of beta-TrCP expression in osteoblasts.Uncoupling of growth plate maturation and bone formation in mice lacking both Schnurri-2 and Schnurri-3Distribution of slow-cycling cells in epiphyseal cartilage and requirement of β-catenin signaling for their maintenance in growth plate.Neogenin regulation of BMP-induced canonical Smad signaling and endochondral bone formation.Functional coupling between the extracellular matrix and nuclear lamina by Wnt signaling in progeria.Looping mediated interaction between the promoter and 3' UTR regulates type II collagen expression in chondrocytes.Estrogen via estrogen receptor beta partially inhibits mandibular condylar cartilage growth.Midkine-deficiency delays chondrogenesis during the early phase of fracture healing in miceWNT-3A modulates articular chondrocyte phenotype by activating both canonical and noncanonical pathwaysMultiple synostoses syndrome is due to a missense mutation in exon 2 of FGF9 gene.Smad1 plays an essential role in bone development and postnatal bone formation.Thyroid hormone-mediated growth and differentiation of growth plate chondrocytes involves IGF-1 modulation of beta-catenin signalingPleiotrophin commits human bone marrow mesenchymal stromal cells towards hypertrophy during chondrogenesisMutant activated FGFR3 impairs endochondral bone growth by preventing SOX9 downregulation in differentiating chondrocytesOsthole stimulates osteoblast differentiation and bone formation by activation of beta-catenin-BMP signaling.Deletion of IFT80 Impairs Epiphyseal and Articular Cartilage Formation Due to Disruption of Chondrocyte Differentiation.Chondrocytes-Specific Expression of Osteoprotegerin Modulates Osteoclast Formation in Metaphyseal BoneSpatial and temporal regulation of gene expression in the mammalian growth plate.Acute alcohol exposure impairs fracture healing and deregulates β-catenin signaling in the fracture callusDefective postnatal endochondral bone development by chondrocyte-specific targeted expression of parathyroid hormone type 2 receptor.CCN1 Regulates Chondrocyte Maturation and Cartilage Development.Inhibition of β-catenin signaling in chondrocytes induces delayed fracture healing in mice.Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects.Activation of beta-catenin signaling in articular chondrocytes leads to osteoarthritis-like phenotype in adult beta-catenin conditional activation mice.PTHrP prevents chondrocyte premature hypertrophy by inducing cyclin-D1-dependent Runx2 and Runx3 phosphorylation, ubiquitylation and proteasomal degradation.Smurf2 induces degradation of GSK-3beta and upregulates beta-catenin in chondrocytes: a potential mechanism for Smurf2-induced degeneration of articular cartilage.GSK-3β function in bone regulates skeletal development, whole-body metabolism, and male life spanAxin2 controls bone remodeling through the beta-catenin-BMP signaling pathway in adult mice.β-catenin activity in late hypertrophic chondrocytes locally orchestrates osteoblastogenesis and osteoclastogenesis.Transient activation of Wnt/{beta}-catenin signaling induces abnormal growth plate closure and articular cartilage thickening in postnatal mice.Role of hypoxia-inducible factor-1alpha in angiogenic-osteogenic coupling.Chondrocyte-specific inhibition of β-catenin signaling leads to dysplasia of the caudal vertebrae in mice.Beta-catenin, cartilage, and osteoarthritis.
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P2860
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 08 April 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@en
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@nl
type
label
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@en
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@nl
prefLabel
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@en
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@nl
P2093
P2860
P356
P1476
Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.
@en
P2093
Brendan F Boyce
Regis J O'Keefe
Tian-Fang Li
Tzong-Jen Sheu
P2860
P304
P356
10.1242/JCS.020362
P407
P577
2008-04-08T00:00:00Z