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A computationally identified compound antagonizes excess FGF-23 signaling in renal tubules and a mouse model of hypophosphatemia

Autor: Jeremy C. Smith, Charles R. Yates, Ai L. Chin, L. Darryl Quarles, Hector A. Velazquez, Jerome Baudry, Zhousheng Xiao, Jesse D. Carrick, Demian Riccardi

Publikováno v: Science signaling. 9(455)

Fibroblast growth factor-23 (FGF-23) interacts with a binary receptor complex composed of α-Klotho (α-KL) and FGF receptors (FGFRs) to regulate phosphate and vitamin D metabolism in the kidney. Excess FGF-23 production, which causes hypophosphatemi

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b7362123b06032b8c971e957ba1ca790
https://pubmed.ncbi.nlm.nih.gov/27923912

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