Wnt signaling in bone development and disease: making stronger bone with Wnts - Wikidata - awgldk - TriplyDB

Wnt signaling in bone development and disease: making stronger bone with Wnts

Wnt signaling in bone development and disease: making stronger bone with Wnts

http://www.wikidata.org/entity/Q36418026

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Chemical Disruption of Wnt-dependent Cell Fate Decision-making Mechanisms in Cancer and Regenerative Medicine Impact of inflammation on the osteoblast in rheumatic diseases Cilia/Ift protein and motor -related bone diseases and mouse models Bipartite recognition of DNA by TCF/Pangolin is remarkably flexible and contributes to transcriptional responsiveness and tissue specificity of wingless signaling Testing models of the APC tumor suppressor/β-catenin interaction reshapes our view of the destruction complex in Wnt signaling Wnt7a Inhibits IL-1β Induced Catabolic Gene Expression and Prevents Articular Cartilage Damage in Experimental Osteoarthritis Wnt-Lrp5 signaling regulates fatty acid metabolism in the osteoblast.Contemporary Approaches for Identifying Rare Bone Disease Causing Genes.The spatiotemporal role of COX-2 in osteogenic and chondrogenic differentiation of periosteum-derived mesenchymal progenitors in fracture repair.Wnt4 signaling prevents skeletal aging and inflammation by inhibiting nuclear factor-κB.SOXC proteins amplify canonical WNT signaling to secure nonchondrocytic fates in skeletogenesis.Wnts produced by Osterix-expressing osteolineage cells regulate their proliferation and differentiation.Function and regulation of primary cilia and intraflagellar transport proteins in the skeleton Role of Wnt signaling in fracture healing Protein kinase A activation enhances β-catenin transcriptional activity through nuclear localization to PML bodies.CXXC5 is a negative-feedback regulator of the Wnt/β-catenin pathway involved in osteoblast differentiation.Small molecule inhibitors of the Dishevelled-CXXC5 interaction are new drug candidates for bone anabolic osteoporosis therapy CCN1 Regulates Chondrocyte Maturation and Cartilage Development.Bone and skeletal muscle: neighbors with close ties Multiple analyses of large-scale genome-wide association study highlight new risk pathways in lumbar spine bone mineral density.Isolation of an ES-Derived Cardiovascular Multipotent Cell Population Based on VE-Cadherin Promoter Activity The role of midkine in skeletal remodelling.Antagonizing miR-218-5p attenuates Wnt signaling and reduces metastatic bone disease of triple negative breast cancer cells.Postsynaptic assembly: a role for Wnt signaling Vitamin D Is a Multilevel Repressor of Wnt/b-Catenin Signaling in Cancer Cells.Strong effect of SNP rs4988300 of the LRP5 gene on bone phenotype of Caucasian postmenopausal women.Short-term application of dexamethasone on stem cells derived from human gingiva reduces the expression of RUNX2 and β-catenin.Bone as a Target Organ in Rheumatic Disease: Impact on Osteoclasts and Osteoblasts.Reverse engineering development: crosstalk opportunities between developmental biology and tissue engineering.Active and water-soluble form of lipidated Wnt protein is maintained by a serum glycoprotein afamin/α-albumin.Molecular characterization of the apical organ of the anthozoan Nematostella vectensis.TNF and Bone Remodeling.Low-Density Lipoprotein Receptor-Related Proteins in Skeletal Development and Disease.Class I PI-3-Kinase Signaling Is Critical for Bone Formation Through Regulation of SMAD1 Activity in Osteoblasts.Use of Primary Calvarial Osteoblasts to Evaluate the Function of Wnt Signaling in Osteogenesis.Wntless spatially regulates bone development through β-catenin-dependent and independent mechanisms.In vitro effect of microRNA-107 targeting Dkk-1 by regulation of Wnt/β-catenin signaling pathway in osteosarcoma.Fatty acid metabolism by the osteoblast.Reduced β-catenin expression affects patterning of bone primordia, but not bone maturation.Exercise and bone health across the lifespan.

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Wnt signaling in bone development and disease: making stronger bone with Wnts

http://www.wikidata.org/entity/Q36418026

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

@zh-my

2012年学术文章

@zh-sg

2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Wnt signaling in bone development and disease: making stronger bone with Wnts

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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CSHPERSPECT.A007997

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Cold Spring Harbor Perspectives in Biology

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Wnt signaling in bone development and disease: making stronger bone with Wnts

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P2093

Bart O Williams

http://www.w3.org/2001/XMLSchema#string

Jean B Regard

http://www.w3.org/2001/XMLSchema#string

Yingzi Yang

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Zhendong Zhong

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P2860

Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)

Osteocyte control of bone formation via sclerostin, a novel BMP antagonist

SOST is a ligand for LRP5/LRP6 and a Wnt signaling inhibitor

Homozygous WNT3 mutation causes tetra-amelia in a large consanguineous family

Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer

Six novel missense mutations in the LDL receptor-related protein 5 (LRP5) gene in different conditions with an increased bone density

Polymorphisms in the sclerosteosis/van Buchem disease gene (SOST) region are associated with bone-mineral density in elderly whites.

Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein

Low-density lipoprotein receptor-related protein 5 (LRP5) is essential for normal cholesterol metabolism and glucose-induced insulin secretion

A mutation in the LDL receptor-related protein 5 gene results in the autosomal dominant high-bone-mass trait

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scholarly article

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10.1101/CSHPERSPECT.A007997

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12

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4

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23209148

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3504445

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