Results 131 to 140 of about 4,164 (178)

Chorein Regulates Key Osteoblast Genes in UMR-106 Cells. [PDF]

Cell Biochem Biophys
Feger M, Tsapara A, Hülße S, Rausch S, Barholz M, Stournaras C, Föller M.   +6 more
europepmc   +1 more source

Genetic reduction or deletion of osteopontin in osteomalacic <i>Hyp</i> mice fails to ameliorate dentoalveolar defects. [PDF]

JBMR Plus
Phanrungsuwan A, Donnelly B, Kim J, Sweet J, de Oliveira FA, Kim DG, Liu ES, Millán JL, McKee MD, Foster BL.   +9 more
europepmc   +1 more source

Clinical and Laboratory Characteristics of Patients with Genetic Rickets: A Single-Center Experience with Long-Term Outcomes. [PDF]

Turk Arch Pediatr
Köprülü Ö, Özer G, Erbaş IM, Nalbantoğlu Ö, Gürsoy S, Özkan B.   +5 more
europepmc   +1 more source

Editorial: Bone metastases in endocrine cancers: advances in diagnosis, treatment, and prevention. [PDF]

Front Endocrinol (Lausanne)
Mandal CC, Rhoades JA.
europepmc   +1 more source

Ontogeny of Phex/PHEX Protein Expression in Mouse Embryo and Subcellular Localization in Osteoblasts† [PDF]

Journal of Bone and Mineral Research, 2002
Abstract PHEX, a phosphate-regulating gene with homologies to endopeptidases on the X chromosome, is mutated in X-linked hypophosphatemia (XLH) in humans and mice (Hyp). Although recent observations indicate that Phex protein is expressed primarily in bone and may play an important role in osteoblast function and bone mineralization, the
Yves Sabbagh, Joseph P Grande, H S Tenenhouse   +2 more
exaly   +3 more sources

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FGF23 is processed by proprotein convertases but not by PHEX

Bone, 2004
X-linked hypophosphatemia (XLH) and autosomal dominant hypophosphatemic rickets (ADHR) are characterized by renal phosphate wasting, rickets, and osteomalacia. ADHR is caused by gain of function mutations in the fibroblast growth factor 23 gene (FGF23). During secretion, FGF23 is processed at the C-terminus between amino acids 179 and 180. The cleavage
Hans Zischka, Kenneth E White
exaly   +3 more sources

PHEX, FGF23, DMP1 and beyond

Current Opinion in Nephrology and Hypertension, 2008
We aim to review the biological properties of novel molecules that are members of a kidney-bone axis involved in the regulation of phosphate homeostasis. In addition, we describe how an improved knowledge of the mechanisms leading to changes in renal phosphate handling may lead to the development of novel therapeutic approaches.As yet, eight genes ...
Tim M, Strom, Harald, Jüppner
openaire   +2 more sources

Inhibition of MEPE cleavage by Phex

Biochemical and Biophysical Research Communications, 2002
X-linked hypophosphatemia (XLH) and the Hyp-mouse disease homolog are caused by inactivating mutations of Phex which results in the local accumulation of an unknown autocrine/paracrine factor in bone that inhibits mineralization of extracellular matrix.
Rong, Guo, Peter S N, Rowe, Shiguang, Liu, Leigh G, Simpson, Zhou-Sheng, Xiao, L Darryl, Quarles   +5 more
openaire   +2 more sources

Downregulation of osteoblast Phex expression by PTH

Bone, 2005
Human/murine X-linked hypophosphatemia is a dominant disorder associated with renal phosphate wasting and defective bone mineralization. This disorder results from mutations in the PHEX/Phex (Phosphate-regulating gene with homologies to endopeptidases on the X chromosome) gene, which is expressed in fully differentiated osteoblasts.
Nathalie, Alos, Brigitte, Ecarot
openaire   +2 more sources