scispace - formally typeset
R

Reinhold G. Erben

Researcher at University of Veterinary Medicine Vienna

Publications -  186
Citations -  9405

Reinhold G. Erben is an academic researcher from University of Veterinary Medicine Vienna. The author has contributed to research in topics: Bone remodeling & Fibroblast growth factor 23. The author has an hindex of 48, co-authored 181 publications receiving 8237 citations. Previous affiliations of Reinhold G. Erben include Harvard University & Ludwig Maximilian University of Munich.

Papers
More filters
Journal ArticleDOI

Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice.

TL;DR: FGF-23 is upstream of the phosphate regulating gene with homologies to endopeptidases on the X chromosome (Phex) and that the increased plasma Fgf-23 levels in Hyp mice (and in XLH patients) may be at least partially responsible for the phosphate imbalance in this disorder.
Journal ArticleDOI

Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor.

TL;DR: The findings clearly establish a molecular role of the VDR in pancreatic insulin synthesis and secretion in vivo and exclude possible influences of hypocalcemia on pancreatic endocrine function.
Journal ArticleDOI

Embedding of Bone Samples in Methylmethacrylate: An Improved Method Suitable for Bone Histomorphometry, Histochemistry, and Immunohistochemistry

TL;DR: The modified MMA embedding process, using commercially available methacrylates can be used without purification, and the histologic quality of bone sections is comparable to that of conventionally MMA-embedded bone specimens.
Journal ArticleDOI

FGF23 regulates renal sodium handling and blood pressure

TL;DR: It is shown that FGF23 directly regulates the membrane abundance of the Na+:Cl− co‐transporter NCC in distal renal tubules by a signaling mechanism involving the FGF receptor/αKlotho complex, extracellular signal‐regulated kinase 1/2 (ERK1/2), serum/glucocorticoid‐regulatedkinase 1 (SGK1), and with‐no lysine kinase‐4 (WNK4
Journal ArticleDOI

Deletion of deoxyribonucleic acid binding domain of the vitamin D receptor abrogates genomic and nongenomic functions of vitamin D.

TL;DR: It is shown that gene-targeted mutant mice express a VDR with an intact hormone binding domain, but lacking the first zinc finger necessary for DNA binding, supporting the conclusion that the classical VDR mediates the nongenomic actions of 1,25-(OH)(2)D(3).