Kenneth E. White, Ph.D.

David D. Weaver Professor of Medical and Molecular Genetics
Chancellor's Professor, IUPUI
  • B.S. Biology 1988, Binghamton University, Vestal NY
  • Ph.D. 1997, Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH  (Fellow of the Albert J. Ryan Foundation)
  • 1997-1999 Postdoctoral Fellow, Indiana University School of Medicine, Department of Medicine, Endocrine Division   (1998-2000, NIH NRSA Postdoctoral Fellow)
  • 1999-2003, Research Associate and Assistant Scientist, Indiana University School of Medicine, Department of Medicine, Endocrine Division
  • 2003-Present, Assistant and Associate Professor. Showalter Scholar and the Dr. David D. Weaver Investigator of Medical and Molecular Genetics; Division Director, Molecular Genetics and Gene Therapy

Dr. White's laboratory is primarily interested in the molecular genetics of metabolic bone diseases. Dr. White played an instrumental role in the positional cloning of the fibroblast growth factor-23 (FGF23) gene and determining that missense mutations in FGF23 are responsible for the human phosphate wasting disorder autosomal dominant hypophosphatemic rickets (ADHR). FGF23 is a novel secreted hormone that may have direct effects on kidney and on bone. We have discovered that recessive, inactivating mutations in FGF23 are responsible for familial tumoral calcinosis (TC), a disorder with a reciprocal phenotype to ADHR. In addition, our group collaboratively determined that mutations in fibroblast growth factor receptor-1 (FGFR1) are responsible for osteoglophonic dysplasia (OGD).

FGF23 is over produced by tumors that cause tumor induced osteomalacia (TIO), a syndrome that is similar to ADHR, indicating that FGF23 is a critical regulator of mineral metabolism. The roles of FGF23 as a growth factor in cancer are unknown, and we are attempting to understand FGF23 regulation in both rare and common disorders. FGF23 is also over produced in the setting of chronic kidney disease (CKD), leading to severe endocrine bone disease.

Several active areas of research are presently being taken. We developed a knock-in animal model of ADHR, and are using in vitro approaches to ask significant questions regarding the roles of FGF23, the FGFRs, and the FGF23 co-receptor Klotho in situations of normal and abnormal mineral metabolism. The experimental designs in Dr. White's lab are undertaken with regard to the long-term goal of application to human disorders as well as for understanding basic bone and renal cell biology. The study of these novel human mutations provides the opportunity to cross disciplines and to widen our understanding of skeletal biology as well as oncology.


Ken White, PhD

 Erica L. Clinkenbeard, PhD; University of Kentucky College of Medicine

Julia Hum, PhD; Indiana University School of Medicine

Pu Ni, Genetics MS Degree student


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. 2015. Endocrinology, in press.

V.S. Tagliabracci, J.L. Engel,  S.E. Wileya, J. Xiao, D. Gonzalez, H. Nidumanda Appaiah, V. Nizeta, K.E. White, and J.E. Dixon. Dynamic regulation of FGF23 by Fam20C phosphorylation, GALNT3 glycosylation, and Furin proteolysis. 2014. Proceedings of the National Academy of Sciences. 111(15):5520-5.

R.C. Smith, L.M. O’Bryan, E.G. Farrow, L.J. Summers, E.L. Clinkenbeard, J.L. Roberts, T.A. Cass,  J. Saha, C. Broderick, Y. L. Ma, Q.Q. Zeng, A. Kharitonenkov, J.M. Wilson, Q. Guo, H. Sun, M.R. Allen, D.B. Burr, M.D. Breyer, and K.E. White. Circulating aKlotho influences phosphate handling by controlling FGF23 production. 2012; Journal of Clinical Investigation, 122(12):4710-5.

E.G. Farrow, X. Yu, L.J. Summers, S.I. Davis, J.C. Fleet, M.R. Allen, A.G. Robling, K.R. Stayrook, V. Jideonwo, M.J. Magers, H.J. Garringer, R. Vidal, R.J. Chan, C.B. Goodwin, S. Hui,  M. Peacock, and K.E. White. Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in Fibroblast growth factor-23 (Fgf23) knock-in mice. 2011; Proceedings of the National Academy of Sciences, 15;108(46):E1146-55.

S.M. Moe, J.S. Radcliffe, K.E. White, V.H. Gattone II,  M.F. Seifert, X. Chen, B. Aldridge, and N.X. Chen. The pathophysiology of early stage chronic kidney disease-mineral bone disorder (CKD-MBD) and response to phosphate binders. 2011; J Bone Miner Res. 26(11):2672-81.

E.G. Farrow and K.E. White, Recent advances in renal phosphate handling. 2010; Nature Reviews Nephrology. 6(4):207-17.

R. Goetz, A. Beenken, O.A. Ibrahimi, J. Kalinina, S.K. Olsen, A.V. Eliseenkova, C. Xu, T. Neubert, F. Zhang, R.J. Linhardt, X. Yu, K.E. White, T. Inagaki, S.A. Kliewer, M. Yamamoto, H. Kurosu, Y. Ogawa, M. Kuro-O, B. Lanske, M.S. Razzaque, M. Mohammadi. Molecular insights into the Klotho-dependent, endocrine mode of action of FGF19 subfamily members. 2007; Molecular and Cellular Biology, 27(9):3417-28.

J.Q. Feng, L.M. Ward, S. Liu, Y. Lu, B. Yuan, X. Yu, F. Rauch, Y. Xie, S.I. Davis, S. Zhang, H. Rios, M.K. Drezner, L.D. Quarles, L.F. Bonewald, and K.E. White. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. 2006; Nature Genetics, 38(11):1310-5.

K.B. Jonsson, R. Zahradnik, T. Larsson, K.E. White, T. Sugimoto, Y. Imanishi, T. Yamamoto, G. Hampson, A. Miyauchi, M. J. Econs, J. Lavigne, and H. Jüppner. Development of an enzyme-linked two-site immunometric assay for FGF-23: elevated circulating concentrations in oncogenic osteomalacia and X-linked hypophosphatemic rickets. 2003; The New England Journal of Medicine, 348(17):1656-1663.

The ADHR consortium.  Group 1. K.E. White, W.E. Evans, J.L.H. O’Riordan, M.C. Speer, M.J. Econs; Group 2. B. Lorenz-Depiereux, M. Grabowski, T. Meitinger, T.M. Strom. Autosomal dominant hypophosphatemic rickets is associated with mutations in FGF23.  2000; Nature Genetics, 26(3), 345-348.

E.L. Clinkenbeard, E.G. Farrow, L.J. Summers, C. Bate, T.A. Cass, M. Peacock, and K.E. White. An early-onset ADHR phenotype is induced by iron deficiency via maternal-neonatal transfer. 2014. J Bone Miner Res. 29(2):361-9.


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