Matrix extracellular phosphoglycoprotein (MEPE) is a new bone renal hormone and vascularization modulator. - Test2 - elhamkhani - TriplyDB

Matrix extracellular phosphoglycoprotein (MEPE) is a new bone renal hormone and vascularization modulator.

Matrix extracellular phosphoglycoprotein (MEPE) is a new bone renal hormone and vascularization modulator.

http://www.wikidata.org/entity/Q33643995

about

ASARM peptides: PHEX-dependent and -independent regulation of serum phosphate Extracellular matrix mineralization in periodontal tissues: Noncollagenous matrix proteins, enzymes, and relationship to hypophosphatasia and X-linked hypophosphatemia Regulation of bone-renal mineral and energy metabolism: the PHEX, FGF23, DMP1, MEPE ASARM pathway A unified model for bone-renal mineral and energy metabolism Novel biological markers of bone: from bone metabolism to bone physiology Increased expression of matrix extracellular phosphoglycoprotein (MEPE) in cortical bone of the rat tibia after mechanical loading: identification by oligonucleotide microarray MEPE is a novel regulator of growth plate cartilage mineralization Bmp2 in osteoblasts of periosteum and trabecular bone links bone formation to vascularization and mesenchymal stem cells.PHEX mimetic (SPR4-peptide) corrects and improves HYP and wild type mice energy-metabolism Abnormal presence of the matrix extracellular phosphoglycoprotein-derived acidic serine- and aspartate-rich motif peptide in human hypophosphatemic dentin.Surface immobilization of MEPE peptide onto HA/β-TCP ceramic particles enhances bone regeneration and remodeling.The bone-vascular axis in chronic kidney disease.A comparative transcriptome analysis identifying FGF23 regulated genes in the kidney of a mouse CKD model.MEPE-derived ASARM peptide inhibits odontogenic differentiation of dental pulp stem cells and impairs mineralization in tooth models of X-linked hypophosphatemia Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling.SPR4-peptide alters bone metabolism of normal and HYP mice.ASARM mineralization hypothesis: a bridge too far?Kbus/Idr, a mutant mouse strain with skeletal abnormalities and hypophosphatemia: identification as an allele of 'Hyp'.Biomineralization of bone: a fresh view of the roles of non-collagenous proteins.Age dependent regulation of bone-mass and renal function by the MEPE ASARM-motif The chicken or the egg: PHEX, FGF23 and SIBLINGs unscrambled.Do ASARM peptides play a role in nephrogenic systemic fibrosis?Overexpression of the DMP1 C-terminal fragment stimulates FGF23 and exacerbates the hypophosphatemic rickets phenotype in Hyp mice.In vivo impact of Dlx3 conditional inactivation in neural crest-derived craniofacial bones Inflammation and functional iron deficiency regulate fibroblast growth factor 23 production.Radiation activated CHK1/MEPE pathway may contribute to microgravity-induced bone density loss.Dietary phosphate restriction suppresses phosphaturia but does not prevent FGF23 elevation in a mouse model of chronic kidney disease.The osteocyte: an endocrine cell ... and more.Increased osteopontin contributes to inhibition of bone mineralization in FGF23-deficient mice.MEPE Localization in the Craniofacial Complex and Function in Tooth Dentin Formation.An in situ hybridization study of perlecan, DMP1, and MEPE in developing condylar cartilage of the fetal mouse mandible and limb bud cartilage.MEPE's diverse effects on mineralization.Inhibition of osteoclastogenesis by mechanically loaded osteocytes: involvement of MEPE.Hypophosphatemia related to paraneoplastic Cushing syndrome in prostate cancer: cure after bilateral adrenalectomy.The phosphate transporter NaPi-IIa determines the rapid renal adaptation to dietary phosphate intake in mouse irrespective of persistently high FGF23 levels.Bone Shaft Revascularization After Marrow Ablation Is Dramatically Accelerated in BSP-/- Mice, Along With Faster Hematopoietic Recolonization.Matrix extracellular phosphoglycoprotein is expressed in causative tumors of oncogenic osteomalacia.Acute Adaption to Oral or Intravenous Phosphate Requires Parathyroid Hormone.

P2860

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P2860

Matrix extracellular phosphoglycoprotein (MEPE) is a new bone renal hormone and vascularization modulator.

http://www.wikidata.org/entity/Q33643995

description

2009 nî lūn-bûn

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2009 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2009 թվականի հունիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年论文

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Matrix extracellular phosphogl ...... and vascularization modulator.

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Matrix extracellular phosphogl ...... and vascularization modulator.

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Matrix extracellular phosphogl ...... and vascularization modulator.

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Aline Martin

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Anne-Marie Hedge

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Peter S N Rowe

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Valentin David

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P2860

Endocrine regulation of energy metabolism by the skeleton

MEPE, a new gene expressed in bone marrow and tumors causing osteomalacia

Human recombinant endopeptidase PHEX has a strict S1' specificity for acidic residues and cleaves peptides derived from fibroblast growth factor-23 and matrix extracellular phosphoglycoprotein

Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia

Degradation of MEPE, DMP1, and release of SIBLING ASARM-peptides (minhibins): ASARM-peptide(s) are directly responsible for defective mineralization in HYP

Renal expression of SIBLING proteins and their partner matrix metalloproteinases (MMPs)

Expression of SIBLINGs and their partner MMPs in salivary glands

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

Recent advances in the renal-skeletal-gut axis that controls phosphate homeostasis

Matrix extracellular phosphoglycoprotein inhibits phosphate transport

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10.1210/EN.2009-0216

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150

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extracellular matrix

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2819738

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