Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone - Wikidata - awgldk - TriplyDB

Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

http://www.wikidata.org/entity/Q28303536

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Wnt/beta-catenin signaling: components, mechanisms, and diseases WISP-1/CCN4 regulates osteogenesis by enhancing BMP-2 activity The Regulatory Roles of MicroRNAs in Bone Remodeling and Perspectives as Biomarkers in Osteoporosis Sclerostin and occlusion: A brief review Crystal structures of the extracellular domain of LRP6 and its complex with DKK1 LRP5 and LRP6 in development and disease The Wnt receptor, Lrp5, is expressed by mouse mammary stem cells and is required to maintain the basal lineage Hesperetin alleviates the inhibitory effects of high glucose on the osteoblastic differentiation of periodontal ligament stem cells Dickkopf-1 regulates bone formation in young growing rodents and upon traumatic injury The genetics of colony form and function in Caribbean Acropora corals The super super-healing MRL mouse strain Lrp4, a novel receptor for Dickkopf 1 and sclerostin, is expressed by osteoblasts and regulates bone growth and turnover in vivo.Promising bone-related therapeutic targets for rheumatoid arthritis.Negative regulation of bone formation by the transmembrane Wnt antagonist Kremen-2.Adiponectin regulates BMSC osteogenic differentiation and osteogenesis through the Wnt/β-catenin pathway Skeletal biology: Where matrix meets mineral SOST and DKK: Antagonists of LRP Family Signaling as Targets for Treating Bone Disease.Wnt5a can both activate and repress Wnt/β-catenin signaling during mouse embryonic development.Aging and bone.Isolation of osteoprogenitors from human jaw periosteal cells: a comparison of two magnetic separation methods.HIV-1 protein induced modulation of primary human osteoblast differentiation and function via a Wnt/β-catenin-dependent mechanism.Lef1DeltaN binds beta-catenin and increases osteoblast activity and trabecular bone mass.Targeting the giant cell tumor stromal cell: functional characterization and a novel therapeutic strategy Effects of constitutive β-catenin activation on vertebral bone growth and remodeling at different postnatal stages in mice Crosstalk between Wnt/β-catenin and estrogen receptor signaling synergistically promotes osteogenic differentiation of mesenchymal progenitor cells.HDAC5 controls MEF2C-driven sclerostin expression in osteocytes.Anti-DKK1 antibody promotes bone fracture healing through activation of β-catenin signaling.Post-natal effect of overexpressed DKK1 on mandibular molar formation Modulation of canonical Wnt signaling by the extracellular matrix component biglycan.The impact of LRP5 polymorphism (rs556442) on calcium homeostasis, bone mineral density, and body composition in Iranian children.CD73-generated adenosine promotes osteoblast differentiation.TGF-β regulates sclerostin expression via the ECR5 enhancer.Missense Mutations in LRP5 Associated with High Bone Mass Protect the Mouse Skeleton from Disuse- and Ovariectomy-Induced Osteopenia.Absence of sclerostin adversely affects B-cell survival.Chemical and genetic evidence for the involvement of Wnt antagonist Dickkopf2 in regulation of glucose metabolism.Targeted overexpression of Dkk1 in osteoblasts reduces bone mass but does not impair the anabolic response to intermittent PTH treatment in mice.Precise regulation of porcupine activity is required for physiological Wnt signaling.Serum levels of sclerostin, Dickkopf-1, and secreted frizzled-related protein-4 are not changed in individuals with high bone mass causing mutations in LRP5.Na+/H+ exchanger regulatory factor 1 (NHERF1) directly regulates osteogenesis.The Influence of DNA Methylation on Bone Cells.

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P2860

Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

http://www.wikidata.org/entity/Q28303536

description

2009 nî lūn-bûn

@nan

2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2009年の論文

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2009年論文

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2009年論文

@zh-hant

2009年論文

@zh-hk

2009年論文

@zh-mo

2009年論文

@zh-tw

2009年论文

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name

Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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type

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

@en

Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Where Wnts went: the exploding field of Lrp5 and Lrp6 signaling in bone

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Molecular cloning and characterization of LR3, a novel LDL receptor family protein with mitogenic activity

Endocrine regulation of energy metabolism by the skeleton

An LRP5 receptor with internal deletion in hyperparathyroid tumors with implications for deregulated WNT/beta-catenin signaling

Autosomal recessive familial exudative vitreoretinopathy is associated with mutations in LRP5.

Mutations in LRP5 or FZD4 underlie the common familial exudative vitreoretinopathy locus on chromosome 11q.

Vascular development in the retina and inner ear: control by Norrin and Frizzled-4, a high-affinity ligand-receptor pair

Patients with high bone mass phenotype exhibit enhanced osteoblast differentiation and inhibition of adipogenesis of human mesenchymal stem cells

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

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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cell surface receptor

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