Reduced affinity to and inhibition by DKK1 form a common mechanism by which high bone mass-associated missense mutations in LRP5 affect canonical Wnt signaling
about
Lrp5 functions in bone to regulate bone massWnt/beta-catenin signaling: components, mechanisms, and diseasesWnts talking with the TGF-β superfamily: WISPers about modulation of osteoarthritisCritical Endothelial Regulation by LRP5 during Retinal Vascular DevelopmentCrystal structures of the extracellular domain of LRP6 and its complex with DKK1Structural and Functional Studies of LRP6 Ectodomain Reveal a Platform for Wnt SignalingStructural Basis of Wnt Signaling Inhibition by Dickkopf Binding to LRP5/6Wnt signaling in bone and musclePotential role for therapies targeting DKK1, LRP5, and serotonin in the treatment of osteoporosisRegulation of Wnt/β-catenin signaling within and from osteocytesLevels of serotonin, sclerostin, bone turnover markers as well as bone density and microarchitecture in patients with high-bone-mass phenotype due to a mutation in Lrp5Epimedium-derived flavonoids modulate the balance between osteogenic differentiation and adipogenic differentiation in bone marrow stromal cells of ovariectomized rats via Wnt/β-catenin signal pathway activationDickkopf-1 regulates bone formation in young growing rodents and upon traumatic injuryPTH stimulates bone formation in mice deficient in Lrp5Targeted disruption of the Wnt regulator Kremen induces limb defects and high bone densityCurrent themes in molecular pediatrics: molecular medicine and its applications.Dickkopf homolog 1 mediates endothelin-1-stimulated new bone formationGeneration and selection of novel fully human monoclonal antibodies that neutralize Dickkopf-1 (DKK1) inhibitory function in vitro and increase bone mass in vivoLrp4, a novel receptor for Dickkopf 1 and sclerostin, is expressed by osteoblasts and regulates bone growth and turnover in vivo.Gene expression analysis in human osteoblasts exposed to dexamethasone identifies altered developmental pathways as putative drivers of osteoporosis.Associations between systemic bone mineral density and early knee cartilage changes in middle-aged adults without clinical knee disease: a prospective cohort study.Clinical and molecular findings in osteoporosis-pseudoglioma syndrome.High systemic bone mineral density increases the risk of incident knee OA and joint space narrowing, but not radiographic progression of existing knee OA: the MOST study.SOST and DKK: Antagonists of LRP Family Signaling as Targets for Treating Bone Disease.Mutations in LRP5 cause primary osteoporosis without features of OI by reducing Wnt signaling activity.Regulation of bone mass by Wnt signaling.An RNA-seq protocol to identify mRNA expression changes in mouse diaphyseal bone: applications in mice with bone property altering Lrp5 mutationsWnt signaling and the control of human stem cell fate.Functional analysis of disease-associated polymorphism LRP5.Q89RCyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.Identification of the first deletion in the LRP5 gene in a patient with autosomal dominant osteopetrosis type IWnt inhibitors Dkk1 and Sost are downstream targets of BMP signaling through the type IA receptor (BMPRIA) in osteoblasts.Fibroblast growth factor 2 stimulation of osteoblast differentiation and bone formation is mediated by modulation of the Wnt signaling pathway.High Bone Mass-Causing Mutant LRP5 Receptors Are Resistant to Endogenous Inhibitors In VivoRelevance of Wnt signaling for osteoanabolic therapy.Missense Mutations in LRP5 Associated with High Bone Mass Protect the Mouse Skeleton from Disuse- and Ovariectomy-Induced Osteopenia.The CCN family member Wisp3, mutant in progressive pseudorheumatoid dysplasia, modulates BMP and Wnt signalingRole of fibroblast growth factor 2 and Wnt signaling in anabolic effects of parathyroid hormone on bone formation.Signaling networks that control the lineage commitment and differentiation of bone cells.Update on Wnt signaling in bone cell biology and bone disease.
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P2860
Reduced affinity to and inhibition by DKK1 form a common mechanism by which high bone mass-associated missense mutations in LRP5 affect canonical Wnt signaling
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Reduced affinity to and inhibi ...... affect canonical Wnt signaling
@en
type
label
Reduced affinity to and inhibi ...... affect canonical Wnt signaling
@en
prefLabel
Reduced affinity to and inhibi ...... affect canonical Wnt signaling
@en
P2093
P2860
P1476
Reduced affinity to and inhibi ...... affect canonical Wnt signaling
@en
P2093
Matthew L Warman
Minrong Ai
Sheri L Holmen
P2860
P304
P356
10.1128/MCB.25.12.4946-4955.2005
P407
P577
2005-06-01T00:00:00Z