Survey of the enthesopathy of X-linked hypophosphatemia and its characterization in Hyp mice - Wikidata - awgldk - TriplyDB

Survey of the enthesopathy of X-linked hypophosphatemia and its characterization in Hyp mice

Survey of the enthesopathy of X-linked hypophosphatemia and its characterization in Hyp mice

http://www.wikidata.org/entity/Q34333904

about

The changing face of hypophosphatemic disorders in the FGF-23 era A clinician's guide to X-linked hypophosphatemia Kbus/Idr, a mutant mouse strain with skeletal abnormalities and hypophosphatemia: identification as an allele of 'Hyp'.Exploring the relationship between entheseal changes and physical activity: a multivariate study.'Sink or swim': an evaluation of the clinical characteristics of individuals with high bone mass Conventional Therapy in Adults With X-Linked Hypophosphatemia: Effects on Enthesopathy and Dental Disease Conventional Therapy in Adults With XLH Improves Dental Manifestations, But Not Enthesopathy Mineralizing enthesopathy is a common feature of renal phosphate-wasting disorders attributed to FGF23 and is exacerbated by standard therapy in hyp mice PTHrP regulates the modeling of cortical bone surfaces at fibrous insertion sites during growth.The role of bone sialoprotein in the tendon-bone insertion.FGF23 and syndromes of abnormal renal phosphate handling Therapeutic management of hypophosphatemic rickets from infancy to adulthood.Disorders of phosphorus homeostasis.Familial hypophosphatemia: an unusual presentation with low back ache, heel pain, and a limp in a young man, and literature review.The expanding family of hypophosphatemic syndromes.Hypophosphatemic rickets: unraveling the role of FGF23.Hypophosphatemic rickets: lessons from disrupted FGF23 control of phosphorus homeostasis.Craniosynostosis-associated Fgfr2(C342Y) mutant bone marrow stromal cells exhibit cell autonomous abnormalities in osteoblast differentiation and bone formation.An atypical degenerative osteoarthropathy in Hyp mice is characterized by a loss in the mineralized zone of articular cartilage.FGF2 High Molecular Weight Isoforms Contribute to Osteoarthropathy in Male Mice.Exome sequencing reveals FAM20c mutations associated with fibroblast growth factor 23-related hypophosphatemia, dental anomalies, and ectopic calcification.

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Survey of the enthesopathy of X-linked hypophosphatemia and its characterization in Hyp mice

http://www.wikidata.org/entity/Q34333904

description

2009 nî lūn-bûn

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2009 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի հուլիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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Carolyn M Macica

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Guoying Liang

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Lee D Katz

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Thomas O Carpenter

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P2860

FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate

Cellular signaling by fibroblast growth factor receptors

Fibroblast growth factor receptor 3 is a negative regulator of bone growth

Where tendons and ligaments meet bone: attachment sites ('entheses') in relation to exercise and/or mechanical load

Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23

Fibroblast growth factor (FGF) 18 signals through FGF receptor 3 to promote chondrogenesis

Klotho converts canonical FGF receptor into a specific receptor for FGF23

MEPE-ASARM peptides control extracellular matrix mineralization by binding to hydroxyapatite: an inhibition regulated by PHEX cleavage of ASARM

A dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice

Mepe, the gene encoding a tumor-secreted protein in oncogenic hypophosphatemic osteomalacia, is expressed in bone

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