FGF23 acts directly on renal proximal tubules to induce phosphaturia through activation of the ERK1/2–SGK1 signaling pathway
Open Access
- 30 September 2012
- journal article
- research article
- Published by Elsevier BV in Bone
- Vol. 51 (3), 621-628
- https://doi.org/10.1016/j.bone.2012.05.015
Abstract
No abstract availableKeywords
Funding Information
- University of Veterinary Medicine Vienna
- Austrian Science Fund (FWF P24186-B21)
- U.S. NIH/NIDDK (DK072944)
- U.S. NIH/NIDCR (DE13686)
This publication has 26 references indexed in Scilit:
- FGF23 induces left ventricular hypertrophyJCI Insight, 2011
- Fibroblast Growth Factor-23-mediated Inhibition of Renal Phosphate Transport in Mice Requires Sodium-Hydrogen Exchanger Regulatory Factor-1 (NHERF-1) and Synergizes with Parathyroid HormoneJournal of Biological Chemistry, 2011
- FGF-23: More than a regulator of renal phosphate handling?Journal of Bone and Mineral Research, 2010
- Klotho: a novel phosphaturic substance acting as an autocrine enzyme in the renal proximal tubuleThe FASEB Journal, 2010
- Isolated C-terminal tail of FGF23 alleviates hypophosphatemia by inhibiting FGF23-FGFR-Klotho complex formationProceedings of the National Academy of Sciences of the United States of America, 2009
- FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1American Journal of Physiology-Renal Physiology, 2009
- Parathyroid hormone inhibits renal phosphate transport by phosphorylation of serine 77 of sodium-hydrogen exchanger regulatory factor–1JCI Insight, 2007
- Klotho converts canonical FGF receptor into a specific receptor for FGF23Nature, 2006
- Suppression of Aging in Mice by the Hormone KlothoScience, 2005
- A new mathematical model for relative quantification in real-time RT-PCRNucleic Acids Research, 2001