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Fanxin Long, PhD
Fanxin Long
Investigator

Bone disorders exact a considerable toll on human health in both children and adults. Dr. Long seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone diseases. His current research includes studies of skeletal stem cells and progenitors, metabolic regulation of bone cells, and the integration of bone and whole-body metabolism.

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Bio

Since the early days of his scientific training, Dr. Long has been interested in understanding how the mammalian skeleton is formed and maintained in a functional state throughout life. Many of his studies have revolved around key developmental pathways such as Hedgehog, Wnt and Notch signaling in bone development and homeostasis. Through mouse genetic studies, his group has defined specific functions of the developmental signals in bone cell differentiation. Their biochemical studies have led to the discovery that developmental signals reprogram cellular metabolism to change cell fate. The lab currently tests the hypothesis that dysregulation of glucose metabolism is a root cause for skeletal disorders associated with diabetes and aging.

Education and Training

BS, Peking University (Cell Biology), 1988

MA, University of California, Santa Barbara (Molecular Biology) 1992

PhD, Tufts University (Developmental Biology), 1997

Titles and Academic Titles

Investigator

Professor of Orthopedic Surgery

William Wikoff Smith Endowed Chair in Pediatric Genomic Research

Professional Memberships

American Society for Bone and Mineral Research, 2003-

Orthopaedic Research Society, 2014-

Professional Awards

Washington University School of Medicine Distinguished Investigator Award, 2009

Publication Highlights

Lee SY and Long F. Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. J Clin Invest. 2018 Oct; pii: 96221. doi: 10.1172/JCI96221
Shi Y, He G, Lee WC, McKenzie JA, Silva MJ and Long F. Gli1 identifies osteogenic progenitors for bone formation and fracture repair. Nat. Comm. 2017 Dec; 8(1):2043. doi: 10.1038/s41467-017-02171-2 PMCID: PMC5725597
Esen E, Chen J, Karner CM, Okunade AL, Patterson BW, Long F. WNT-LRP5 signaling induces Warburg effect through mTORC2 activation during osteoblast differentiation. Cell Metab. 2013 May; 17(5):745-55. doi: 10.1016/j.cmet.2013.03.017. Epub 2013 Apr 25. PMCID: PMC3653292
Wu X, Tu X, Joeng KS, Hilton MJ, Williams DA, Long F. Rac1 activation controls nuclear localization of b-catenin during canonical Wnt signaling. Cell. 2008 Apr; 133(2):340-53. doi: 10.1016/j.cell.2008.01.052 PMCID: PMC2390926
Hilton MJ, Tu X, Wu X, Bai S, Zhao H, Kobayashi T, Kronenberg HM, Teitelbaum SL, Ross FP, Kopan R, Long F. Notch signaling maintains bone marrow mesenchymal progenitors by suppressing osteoblast differentiation. Nat Med. 2008 Mar; 14(3):306-14. doi: 10.1038/nm1716. Epub 2008 Feb 24. PMCID: PMC2740725