Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia.

By Y. Yamazaki, R. Okazaki, M. Shibata, Y. Hasegawa, K. Satoh, T. Tajima, Y. Takeuchi, T. Fujita, K. Nakahara, T. Yamashita and 1 more. Journal of Clinical Endocrinology and Metabolism, 2002

655 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology, Physiology

View Paper: https://www.semanticscholar.org/paper/ad93a4e168abc316b9f53d00e7291d4aa0cdc696

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. A. Beenken
2. M. Mohammadi
3. H. Jüppner
4. D. Bikle

In Nephrology

1. M. Mohammadi
2. A. Beenken
3. D. Bikle

Citations in the corpus

• Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. (2003, background): “However, recently published data suggest a short half-life of intact FGF-23 in tumor-induced osteomalacia, which does not support the latter hypothesis [12].”
• The FGF family: biology, pathophysiology and therapy (2009, positive): “By an unknown mechanism, this leads to increased FGF23 levels in many patients with this diseas”
• FGF‐23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis (2003, methodology): “phosphate and FGF-23 levels using an ELISA system for human full-length FGF-23,((9)) whose antibodies recognize 430 SHIMADA ET AL.”
• Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006, background): “On the basis of these observations, it would be interesting to determine whether treatment with active vitamin D analogues causes similar increments in FGF23 levels in patients with XLH and explains the variation in FGF23 levels that is observed in these patients (7).”