Ken White Lab

The White Laboratory, led by Ken White, PhD, is studying the molecular genetics of metabolic bone diseases involving the osteocyte-derived hormone fibroblast growth factor-23 (FGF23).

Mutations in FGF23 are responsible for the human phosphate wasting disorder autosomal dominant hypophosphatemic rickets (ADHR) and the converse disorder hyperphosphatemic familial tumoral calcinosis (hfTC). Studies in knock in and conditional animal models developed in the White lab, as well as in cell culture, are underway to elicit the factors controlling FGF23 production and to understand its bioactivity via the co-receptor KLOTHO.

Get Research Updates

To stay up-to-date on the medical research work at IU School of Medicine, follow the IU School of Medicine research blog, where investigators throughout the school’s academic departments statewide post updates about their work.

Blogs Hub

Active Research

  • National Institute of Health R01, (NIDDK) DK095784: "Control of FGF23 Bioactivity via Circulating alpha-Klotho"
    The goals of this project are to understand the function of soluble isoforms of the FGF23 co-receptor Klotho.
  • NIH-NIAMS R21 AR070329-01: "Novel mediators of FGF23 bioactivity"
    The goal of this proposal is to test novel kidney FGF23-Klotho signaling pathways.
  • Indiana Center for Musculoskeletal Health Pilot proposal: "Overriding FGF23 in CKD: Improving translational outcomes"
    The goal of this proposal is to generate pilot data for integrated, larger proposals in CKD and metabolic bone disease. (White, Allen, Moe co-PI)
  • Marian University Faculty Research Development Grant Program, "Cell-Specific targeting to control FGF23 bioactivity"
    The goal of this proposal is to test new hypotheses on the regulation of FGF23 in vivo.

Recent Publications

A full listing of publications by Ken White, PhD is available.
  • 2017

    J.M. Hum, E.L. Clinkenbeard, C. Ip, T.A. Cass, M.R. Allen, and K.E. White. The metabolic bone disease associated with the Hyp mutation is independent of osteoblastic HIF1α expression. 2017. Bone Reports; 6:38-43. PMID: 28377980; PMCID: PMC5365303.

    E.L. Clinkenbeard, K.R. Stayrook, H.N.Appaiah, M.R. Hanudel, E.G. Farrow, T.A. Cass, L.J. Summers, C.S. Ip, J.M. Hum, J.C. Thomas, M. Ivan, B.R. Richine, R.J. Chan, T.L. Clemens, E. Schipani, Y. Sabbagh, L. Xu, E.F. Srour, M.B. Alvarez, M.A. Kacena, I.B. Salusky, T. Ganz, E. Nemeth and K.E. White. Erythropoietin (EPO) Induces Fibroblast growth factor-23 (FGF23), revealing novel roles for bone and bone marrow in renal failure. 2017. Hematologica, In press. PMID: 28818868; DOI: 10.3324/haematol.2017.167882.

  • 2016

    J.C. Fleet, R.A. Replogle, P. Reyes-Fernandez, L. Wang, M. Zhang, E.L. Clinkenbeard, and K.E. White. Gene-by-diet interactions affect serum 1,25 dihydroxyvitamin D levels in male BXD recombinant inbred mice. 2016. Endocrinology, 157(2):470-81. PMID: 26587785; PMCID: PMC4733130.

    E.L. Clinkenbeard, T.A. Cass, P. Ni, J.M. Hum, T. Bellido, M.R. Allen, and K.E. White. Conditional deletion of murine Fgf23: Interruption of the normal skeletal responses to phosphate challenge and rescue of genetic hypophosphatemia. 2016. J Bone Mineral Rsch, 31(6):1247-57. PMID: 26792657; PMCID: PMC4891276.

    J.M. Hum, L.M. O’Bryan, E.L. Clinkenbeard, R.C. Smith, and K.E. White. A soluble form of αKlotho prevents aortic calcification and disease phenotypes during chronic hyperphosphatemia. 2016. JASN; 28(4):1162-1174. PMID: 27837149; PMCID: PMC5373441.

Research Team

Erica L. Clinkenbeard, PhD

Assistant Professor of Medical and Molecular Genetics

Additional Research Team Members

Other research team members in the Ken White lab include Megan Noonan, MS; Pu Ni; and Katie Philo.