Fanxin Long

faculty photo
Professor of Orthopaedic Surgery
Department: Orthopaedic Surgery
Graduate Group Affiliations

Contact information
The Children's Hospital of Philadelphia, Abramson Research Center 902A
3615 Civic Center Blvd
Philadelphia, PA 19104
Education:
B.S. (Cell Biology)
Peking University, 1988.
M.A. (Biochemistry and Molecular Biology)
University of California, Santa Barbara, 1992.
Ph.D. (Developmental Biology)
Tufts University School of Medicine, 1997.
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Description of Research Expertise

Research Interests
The Long lab seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone disorders.

Key Words
Metabolism, mesenchymal stem cells, diabetes, aging, skeletal development

Research Details
Much of the research to date has centered around the role and mechanism of key developmental signals such as Hh, Wnt and Notch in regulating skeletal cell differentiation and function. Through mouse genetic studies, the lab has defined specific functions of the developmental signals in osteoblast differentiation. Their biochemical studies have led to the discovery that the developmental signals control cell fate decisions in part through reprograming cellular metabolism. The lab currently tests the hypothesis that dysregulation of glucose metabolism is a root cause for skeletal disorders associated with diabetes and aging. In other projects, the lab studies the cross-regulation between bone and whole-body metabolism, and also uses lineage-tracing and single-cell technologies to identify skeletal stem cells and progenitors in the mouse.

Rotation Projects
Genetic and chemical approaches to study metabolic regulation of skeletal cells in vitro
Morphometric studies of bone phenotypes in genetically modified mice

Selected Publications

Seung-Yon Lee and Fanxin Long: Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. Journal of Clinical Investigation Nov. 2018 pii: 96221. doi: 10.1172/JCI96221.

Lee SY, Abel ED, Long F: Glucose metabolism induced by Bmp signaling is essential for murine skeletal development. Nat Commun. 9(1): 4831, Nov. 2018.

Yu Shi, Guangxu He, Wen-Chih Lee, Jenny A. McKenzie, Matthew J. Silva, Fanxin Long: Gli1 identifies osteogenic progenitors for bone formation and fracture repair. Nat Commun. 8(1): 2043, 12 2017.

Karner Courtney M, Esen Emel, Chen Jiakun, Hsu Fong-Fu, Turk John, Long Fanxin: Wnt Protein Signaling Reduces Nuclear Acetyl-CoA Levels to Suppress Gene Expression during Osteoblast Differentiation. The Journal of biological chemistry 291(25): 13028-39, Jun 2016.

Shi Y, Chen J, Karner CM and Long F. : Hedgehog signaling activates a positive feedback mechanism involving insulin-like growth factors to induce osteoblast differentiation. PNAS 112(15): 4678-4683, March 2015.

Karner Courtney M, Esen Emel, Okunade Adewole L, Patterson Bruce W, Long Fanxin: Increased glutamine catabolism mediates bone anabolism in response to WNT signaling. The Journal of clinical investigation 125(2): 551-62, Feb 2015.

Emel Esen, Jianquan Chen, Courtney M. Karner, Adewole L. Okunade, Bruce W. Patterson, Fanxin Long. : WNT-LRP5 signaling induces Warburg effect through mTORC2 activation during osteoblast differentiation. Cell Metab. 17(5): 745-755, May 2013.

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 133(2): 340-353, April 2008.

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 14(3): 306-314, March 2008.

Tu X, Joeng KS, Nakayama KI, Nakayama K, Rajagopal J, Carroll TJ, McMahon AP, Long F. : Noncanonical Wnt signaling through G protein-linked Pkcdelta activation promotes bone formation. Dev Cell 12(1): 113-127, January 2007.

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Last updated: 12/22/2018
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