A computationally identified compound antagonizes excess FGF-23 signaling in renal tubules and a mouse model of hypophosphatemia-Reference-Cited by-同舟云学术

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

Published:2016-11-22 Issue:455 Volume:9 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Xiao Zhousheng¹,Riccardi Demian²³,Velazquez Hector A.³⁴,Chin Ai L.⁵,Yates Charles R.⁶,Carrick Jesse D.⁵,Smith Jeremy C.³⁴,Baudry Jerome³⁴,Quarles L. Darryl¹

Affiliation:

1. Department of Medicine, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38165, USA.

2. Department of Chemistry, Earlham College, 801 National Road West, Richmond, IN 47374, USA.

3. Department of Biochemistry and Cellular and Molecular Biology, University of Tennessee, Knoxville, TN 37996, USA.

4. University of Tennessee/Oak Ridge National Laboratory Center for Molecular Biophysics, Oak Ridge National Laboratory, 1 Bethel Valley Road, Oak Ridge, TN 37830, USA.

5. Department of Chemistry, Tennessee Technological University, 55 University Drive, Cookeville, TN 38501, USA.

6. Department of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN 38163, USA.

Abstract

A ligand-targeted compound may alleviate hypophosphatemia-associated metabolic deficiencies in patients with excess production of FGF-23.

Funder

National Institute of Arthritis and Musculoskeletal and Skin Diseases

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference114 articles.

1. Hormone-like (endocrine) Fgfs: their evolutionary history and roles in development, metabolism, and disease

2. Regulation of Fibroblastic Growth Factor 23 Expression but Not Degradation by PHEX

3. Evidence for a bone-kidney axis regulating phosphate homeostasis

4. Pathogenic role of Fgf23 in Hyp mice

5. Pathogenic role of Fgf23 in Dmp1-null mice

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