Disruption of Lrp4 function by genetic deletion or pharmacological blockade increases bone mass and serum sclerostin levels - Wikidata - awgldk - TriplyDB

Disruption of Lrp4 function by genetic deletion or pharmacological blockade increases bone mass and serum sclerostin levels

Disruption of Lrp4 function by genetic deletion or pharmacological blockade increases bone mass and serum sclerostin levels

http://www.wikidata.org/entity/Q34661015

about

Sclerostin Inhibition in the Management of Osteoporosis From disease to treatment: from rare skeletal disorders to treatments for osteoporosis Modulating Bone Resorption and Bone Formation in Opposite Directions in the Treatment of Postmenopausal Osteoporosis Wnt signaling in bone and muscle Lrp4 in osteoblasts suppresses bone formation and promotes osteoclastogenesis and bone resorption The regulation of osteoclast differentiation by Wnt signals Osteocytes and Skeletal Pathophysiology Deletion of Rac in Mature Osteoclasts Causes Osteopetrosis, an Age-Dependent Change in Osteoclast Number, and a Reduced Number of Osteoblasts In Vivo.Osteoblastic Lrp4 promotes osteoclastogenesis by regulating ATP release and adenosine-A2AR signaling.Genetic Approaches To Identifying Novel Osteoporosis Drug Targets.Appropriate models for novel osteoporosis drug discovery and future perspectives.Regulation of bone metabolism by Wnt signals.Multiple modes of Lrp4 function in modulation of Wnt/β-catenin signaling during tooth development.The Lrp4R1170Q Homozygous Knock-In Mouse Recapitulates the Bone Phenotype of Sclerosteosis in Humans.Microgravity Stress: Bone and Connective Tissue.Role and mechanism of action of sclerostin in bone.Osteocytic signalling pathways as therapeutic targets for bone fragility.A Novel Domain-Specific Mutation in a Sclerosteosis Patient Suggests a Role of LRP4 as an Anchor for Sclerostin in Human Bone.How rare bone diseases have informed our knowledge of complex diseases.Hormonal and systemic regulation of sclerostin.Low-Density Lipoprotein Receptor-Related Proteins in Skeletal Development and Disease.Bone corticalization requires local SOCS3 activity and is promoted by androgen action via interleukin-6.Osteocyte regulation of bone and blood.Musculoskeletal Health in the Context of Spinal Cord Injury.Role of the Wnt/β-Catenin Pathway in Renal Osteodystrophy.

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P2860

Disruption of Lrp4 function by genetic deletion or pharmacological blockade increases bone mass and serum sclerostin levels

http://www.wikidata.org/entity/Q34661015

description

2014 nî lūn-bûn

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2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2014 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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PNAS.1413828111

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Proceedings of the National Academy of Sciences of the United States of America

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Disruption of Lrp4 function by ...... ss and serum sclerostin levels

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Bernd Kinzel

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

Ina Kramer

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Michaela Kneissel

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Ming-Kang Chang

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Olivier Leupin

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Sabine Guth-Gundel

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Thomas Huber

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P2860

WNT16 influences bone mineral density, cortical bone thickness, bone strength, and osteoporotic fracture risk

Twenty bone-mineral-density loci identified by large-scale meta-analysis of genome-wide association studies

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

Bone overgrowth-associated mutations in the LRP4 gene impair sclerostin facilitator function

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

LRP4 mutations alter Wnt/beta-catenin signaling and cause limb and kidney malformations in Cenani-Lenz syndrome

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

NMR structure of the Wnt modulator protein Sclerostin

Wnt antagonists bind through a short peptide to the first β-propeller domain of LRP5/6

A 52-kb deletion in the SOST-MEOX1 intergenic region on 17q12-q21 is associated with van Buchem disease in the Dutch population

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10.1073/PNAS.1413828111

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