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

Endocrine regulation of energy metabolism by the skeleton

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MEPE, a New Gene Expressed in Bone Marrow and Tumors Causing Osteomalacia

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Effects of Aldosterone on the Vasculature

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Mouse α1(I)‐collagen promoter is the best known promoter to drive efficient Cre recombinase expression in osteoblast

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Targeted Disruption of the Osteoblast/Osteocyte Factor 45 Gene (OF45) Results in Increased Bone Formation and Bone Mass

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Angiotensin II accelerates osteoporosis by activating osteoclasts

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MEPE has the properties of an osteoblastic phosphatonin and minhibin

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Dentin Matrix Protein 1 (DMP1): New and Important Roles for Biomineralization and Phosphate Homeostasis

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Octreotide Therapy for Tumor-Induced Osteomalacia

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

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Tumors Associated With Oncogenic Osteomalacia Express Genes Important in Bone and Mineral Metabolism

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Aberrant Phex function in osteoblasts and osteocytes alone underlies murine X-linked hypophosphatemia

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Expression of SIBLINGs and Their Partner MMPs in Salivary Glands

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Activation of Renin-Angiotensin System Induces Osteoporosis Independently of Hypertension

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Degradation of MEPE, DMP1, and release of SIBLING ASARM-Peptides (Minhibins): ASARM-Peptide(s) are directly responsible for defective mineralization in HYP

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Bone morphogenetic protein receptor signaling is necessary for normal murine postnatal bone formation

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T he W rickkened P athways of FGF23, MEPE and PHEX

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MEPE, the Gene Encoding a Tumor-Secreted Protein in Oncogenic Hypophosphatemic Osteomalacia, Is Expressed in Bone

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Surface plasmon resonance (SPR) confirms that MEPE binds to PHEX via the MEPE-ASARM motif: a model for impaired mineralization in X-linked rickets (HYP)

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

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The relationship between bone metastasis from human breast cancer and integrin alpha(v)beta3 expression.

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Matrix extracellular phosphoglycoprotein (MEPE) is highly expressed in osteocytes in human bone

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Serum MEPE-ASARM-peptides are elevated in X-linked rickets (HYP): implications for phosphaturia and rickets

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Renal Calcification in Mice Homozygous for the Disrupted Type IIa Na/Pi Cotransporter Gene Npt2

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PHEX, FGF23, DMP1 and beyond

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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

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Phosphorylated acidic serine–aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity

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Aldosterone Enhances Ischemia-Induced Neovascularization Through Angiotensin II–Dependent Pathway

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High-Resolution Three-Dimensional Micro-Computed Tomography Detects Bone Loss and Changes in Trabecular Architecture Early

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Two-week longitudinal survey of bone architecture alteration in the hindlimb-unloaded rat model of bone loss: sex differences

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DMP1 and MEPE expression are elevated in osteocytes after mechanical loading in vivo: theoretical role in controlling mineral quality in the perilacunar matrix.

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

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Matrix Extracellular Phosphoglycoprotein Inhibits Phosphate Transport

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Serum Levels of Matrix Extracellular Phosphoglycoprotein (MEPE) in Normal Humans Correlate with Serum Phosphorus, Parathyroid Hormone and Bone Mineral Density

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Preconditioning of the distal tubular epithelium of the human kidney precedes nephrocalcinosis

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Correction of the mineralization defect in hyp mice treated with protease inhibitors CA074 and pepstatin

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Matrix extracellular phosphoglycoprotein causes phosphaturia in rats by inhibiting tubular phosphate reabsorption

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Regulation of Osteoclast Differentiation and Function by Phosphate: Potential Role of Osteoclasts in the Skeletal Abnormalities in Hypophosphatemic Conditions

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The osteoclast generation: an in vitro and in vivo study with a genetically labelled avian monocytic cell line

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Expression Analysis of Fibroblast Growth Factor-23, Matrix Extracellular Phosphoglycoprotein, Secreted Frizzled-Related Protein-4, and Fibroblast Growth Factor-7: Identification of Fibroblast Growth Factor-23 and Matrix Extracellular Phosphoglycoprotein as Major Factors Involved in Tumor-Induced Osteomalacia

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Aberrant Phex function in osteoblasts and osteocytes alone underlies murine X-linked hypophosphatemia

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Increased cathepsin D release byHypmouse osteoblast cells

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Role of abnormal neutral endopeptidase-like activities inHyp mouse bone cells in renal phosphate transport

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Oncogenic osteomalacia, a rare paraneoplastic syndrome due to phosphate wasting – A case report and review of the literature

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Matrix extracellular phosphoglycoprotein (MEPE) correlates with serum phosphorus prior to and during octreotide treatment and following excisional surgery in hypophosphatemic linear sebaceous nevus syndrome

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Impaired Energetic Metabolism After Central Leptin Signaling Leads to Massive Appendicular Bone Loss in Hindlimb-Suspended Rats

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Altered cathepsin D metabolism in PHEX antisense human osteoblast cells

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The Osteocyte: An Endocrine Cell … and More

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Inflammation and functional iron deficiency regulate fibroblast growth factor 23 production

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Bone proteins PHEX and DMP1 regulate fibroblastic growth factor <i>Fgf23</i> expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling

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The importance of the SIBLING family of proteins on skeletal mineralisation and bone remodelling

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A Comparative Transcriptome Analysis Identifying FGF23 Regulated Genes in the Kidney of a Mouse CKD Model

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Regulation of bone-renal mineral and energy metabolism: the PHEX, FGF23, DMP1, MEPE ASARM pathway

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Novel biological markers of bone: from bone metabolism to bone physiology

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Endocrine role of bone: recent and emerging perspectives beyond osteocalcin

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Inhibition of Osteoclastogenesis by Mechanically Loaded Osteocytes: Involvement of MEPE

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Increased Osteopontin Contributes to Inhibition of Bone Mineralization in FGF23-Deficient Mice

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The role of the SIBLING, Bone Sialoprotein in skeletal biology — Contribution of mouse experimental genetics

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Microcalcifications in breast cancer: Lessons from physiological mineralization

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Bone mineralization

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Structure and quantification of microvascularisation within mouse long bones: What and how should we measure?

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RNA sequencing-based analysis of the laying hen uterus revealed the novel genes and biological pathways involved in the eggshell biomineralization

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Extracellular matrix mineralization in periodontal tissues: Noncollagenous matrix proteins, enzymes, and relationship to hypophosphatasia and X‐linked hypophosphatemia

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MEPE-Derived ASARM Peptide Inhibits Odontogenic Differentiation of Dental Pulp Stem Cells and Impairs Mineralization in Tooth Models of X-Linked Hypophosphatemia

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Bmp2 gene in osteoblasts of periosteum and trabecular bone links bone formation to vascularization and mesenchymal stem cells

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Fibroblast growth factor 23 and its role in phosphate homeostasis

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The chicken or the egg: PHEX, FGF23 and SIBLINGs unscrambled

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MEPE’s Diverse Effects on Mineralization

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ASARM peptides: PHEX-dependent and -independent regulation of serum phosphate

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Acute Adaption to Oral or Intravenous Phosphate Requires Parathyroid Hormone

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The Regulatory Role of Matrix Proteins in Mineralization of Bone

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The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

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MEPE is a novel regulator of growth plate cartilage mineralization

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Interactions between osteopontin and vascular endothelial growth factor: Implications for cancer

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News on Biomarkers in CKD‐MBD

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Bone Matrix Proteins and Mineralization Process

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The bone–vascular axis in chronic kidney disease

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Overexpression of the DMP1 C-Terminal Fragment Stimulates FGF23 and Exacerbates the Hypophosphatemic Rickets Phenotype in Hyp Mice

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FAM20C Overview: Classic and Novel Targets, Pathogenic Variants and Raine Syndrome Phenotypes

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