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Fanxin Long, Ph.D.
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Professor of Orthopaedic Surgery
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Department: Orthopaedic Surgery
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The Children's Hospital of Philadelphia, Abramson Research Center 902A
39 3615 Civic Center Blvd
Philadelphia, PA 19104
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39 3615 Civic Center Blvd
Philadelphia, PA 19104
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Email:
longf1@chop.edu
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longf1@chop.edu
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Publications
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Education:
21 9 B.S. 19 (Cell Biology) c
2a Peking University, 1988.
21 9 M.A. 2f (Biochemistry and Molecular Biology) c
40 University of California, Santa Barbara, 1992.
21 a Ph.D. 22 (Developmental Biology) c
3c Tufts University School of Medicine, 1997.
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21 9 B.S. 19 (Cell Biology) c
2a Peking University, 1988.
21 9 M.A. 2f (Biochemistry and Molecular Biology) c
40 University of California, Santa Barbara, 1992.
21 a Ph.D. 22 (Developmental Biology) c
3c Tufts University School of Medicine, 1997.
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Links
e1 Search PubMed for articles
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Permanent linke1 Search PubMed for articles
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9d The Long lab seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone disorders.
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11 Key Words
c3 mesenchymal stem/progenitor cells, metabolic and epigenetic regulation, skeletal cell differentiation and function, diabetic osteopenia, skeletal aging, bone development and regeneration
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18 Research Details
520 Skeletal diseases, ranging from congenital dysplasia to osteosarcoma to osteoarthritis and osteoporosis, take a significant toll on human health. The overarching goal of our research is to discover key steps in the molecular or metabolic regulation of skeletal cell differentiation or function, with the hope of uncovering therapeutic targets for treating the various skeletal diseases. Many of our studies have centered around the role and mechanism of key developmental signals such as Hh, Wnt, Notch and Bmp in regulating skeletal development and homeostasis. Through mouse genetic studies, we have defined specific functions of the developmental signals in bone and cartilage cell differentiation. Our molecular and biochemical studies have led to the discovery that the developmental signals alter cell fate and activity in part through reprograming of the cellular metabolism of major energy substrates. Recently, the lab has identified cell-intrinsic disruption of glucose metabolism as a pathogenic basis for osteoarthritis and diabetic osteopenia. In other projects, we combine single-cell sequencing technology with genetic lineage-tracing or functional studies to identify skeletal stem/progenitor cells in the mouse, and to examine their contribution to bone maintenance or pathology.
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19 Rotation Projects
4c Metabolic and epigenetic reprogramming during cell differentiation
60 Functional dissection of metabolic pathways in the skeleton of genetically modified mice
41 Lineage tracing of skeletal stem/progenitor cells in vivo
29 Other projects open for discussion
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Description of Research Expertise
23 Research Interests9d The Long lab seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone disorders.
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11 Key Words
c3 mesenchymal stem/progenitor cells, metabolic and epigenetic regulation, skeletal cell differentiation and function, diabetic osteopenia, skeletal aging, bone development and regeneration
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18 Research Details
520 Skeletal diseases, ranging from congenital dysplasia to osteosarcoma to osteoarthritis and osteoporosis, take a significant toll on human health. The overarching goal of our research is to discover key steps in the molecular or metabolic regulation of skeletal cell differentiation or function, with the hope of uncovering therapeutic targets for treating the various skeletal diseases. Many of our studies have centered around the role and mechanism of key developmental signals such as Hh, Wnt, Notch and Bmp in regulating skeletal development and homeostasis. Through mouse genetic studies, we have defined specific functions of the developmental signals in bone and cartilage cell differentiation. Our molecular and biochemical studies have led to the discovery that the developmental signals alter cell fate and activity in part through reprograming of the cellular metabolism of major energy substrates. Recently, the lab has identified cell-intrinsic disruption of glucose metabolism as a pathogenic basis for osteoarthritis and diabetic osteopenia. In other projects, we combine single-cell sequencing technology with genetic lineage-tracing or functional studies to identify skeletal stem/progenitor cells in the mouse, and to examine their contribution to bone maintenance or pathology.
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19 Rotation Projects
4c Metabolic and epigenetic reprogramming during cell differentiation
60 Functional dissection of metabolic pathways in the skeleton of genetically modified mice
41 Lineage tracing of skeletal stem/progenitor cells in vivo
29 Other projects open for discussion
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10f Song F, Lee WD, Marmo T, Ji X, Song C, Liao X, Seeley R, Yao L, Liu H, Long F: Osteoblast-intrinsic defect in glucose metabolism impairs bone formation in type II diabetic male mice. Elife May 2023.
12f Li K, Ji X, Seeley R, Lee WC, Shi Y, Song F, Liao X, Song C, Huang X, Rux D, Cao J, Luo X, Anderson SM, Huang W, Long F: Impaired glucose metabolism underlies articular cartilage degeneration in osteoarthritis. FASEB J. June 2022.
d2 Lee WC, Ji X, Nissim I, Long F.: Malic Enzyme Couples Mitochondria with Aerobic Glycolysis in Osteoblasts. Cell Rep 32: 108108, Sep 2020.
f8 Seung-Yon Lee and Fanxin Long: Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. JCI 128(12): 5573, Dec. 2018.
de 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.
10d 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, Dec 2017.
11d 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.
f6 Chen J. and Long F.: mTORC1 signaling critically controls mammalian skeletal growth through stimulation of protein synthesis. Development 141(14): 2848-2854, July 2014.
13f 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.
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Selected Publications
120 Ji X, Seeley R, Li K, Song F, Liao X, Song C, Angelozzi M, Valeri A, Marmo T, Lee WC, Shi Y, Long F: Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes. Cell Chem Biol. July 2023.10f Song F, Lee WD, Marmo T, Ji X, Song C, Liao X, Seeley R, Yao L, Liu H, Long F: Osteoblast-intrinsic defect in glucose metabolism impairs bone formation in type II diabetic male mice. Elife May 2023.
12f Li K, Ji X, Seeley R, Lee WC, Shi Y, Song F, Liao X, Song C, Huang X, Rux D, Cao J, Luo X, Anderson SM, Huang W, Long F: Impaired glucose metabolism underlies articular cartilage degeneration in osteoarthritis. FASEB J. June 2022.
d2 Lee WC, Ji X, Nissim I, Long F.: Malic Enzyme Couples Mitochondria with Aerobic Glycolysis in Osteoblasts. Cell Rep 32: 108108, Sep 2020.
f8 Seung-Yon Lee and Fanxin Long: Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. JCI 128(12): 5573, Dec. 2018.
de 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.
10d 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, Dec 2017.
11d 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.
f6 Chen J. and Long F.: mTORC1 signaling critically controls mammalian skeletal growth through stimulation of protein synthesis. Development 141(14): 2848-2854, July 2014.
13f 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.
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