BRENDAN BOYCE

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. pmc Advances in osteoclast biology reveal potential new drug targets and new roles for osteoclasts
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    J Bone Miner Res 28:711-22. 2013
  2. doi request reprint The osteoclast, bone remodelling and treatment of metabolic bone disease
    Brendan F Boyce
    Department ofPathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Eur J Clin Invest 42:1332-41. 2012
  3. pmc TNF inhibits production of stromal cell-derived factor 1 by bone stromal cells and increases osteoclast precursor mobilization from bone marrow to peripheral blood
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Arthritis Res Ther 10:R37. 2008
  4. pmc Increased lymphangiogenesis in joints of mice with inflammatory arthritis
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Arthritis Res Ther 9:R118. 2007
  5. ncbi request reprint TNF-alpha and pathologic bone resorption
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Keio J Med 54:127-31. 2005
  6. ncbi request reprint New roles for osteoclasts in bone
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Ann N Y Acad Sci 1116:245-54. 2007
  7. ncbi request reprint Roles for NF-kappaB and c-Fos in osteoclasts
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    J Bone Miner Metab 23:11-5. 2005
  8. ncbi request reprint The RANKL/RANK/OPG pathway
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Curr Osteoporos Rep 5:98-104. 2007
  9. ncbi request reprint Osteoclast precursors: cytokine-stimulated immunomodulators of inflammatory bone disease
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA
    Curr Opin Rheumatol 18:427-32. 2006
  10. ncbi request reprint Future anti-catabolic therapeutic targets in bone disease
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY, 14642, USA
    Ann N Y Acad Sci 1068:447-57. 2006

Research Grants

  1. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 1999
  2. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2009
  3. 2007 Bones and Teeth Gordon Research Conference
    BRENDAN BOYCE; Fiscal Year: 2007
  4. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2007
  5. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2006
  6. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2005
  7. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2004
  8. RANK/NF-KappaB signaling in chondrogenesis
    BRENDAN BOYCE; Fiscal Year: 2003
  9. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2002
  10. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2001

Detail Information

Publications52

  1. pmc Advances in osteoclast biology reveal potential new drug targets and new roles for osteoclasts
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    J Bone Miner Res 28:711-22. 2013
    ..This article reviews current understanding of how bone resorption is regulated both positively and negatively in normal and pathologic states...
  2. doi request reprint The osteoclast, bone remodelling and treatment of metabolic bone disease
    Brendan F Boyce
    Department ofPathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Eur J Clin Invest 42:1332-41. 2012
    ..Diseases associated with increased bone resorption have increased remodelling often with inadequate bone formation and increased risk of fracture. New therapies are needed for these diseases to reduce resorption and increase formation...
  3. pmc TNF inhibits production of stromal cell-derived factor 1 by bone stromal cells and increases osteoclast precursor mobilization from bone marrow to peripheral blood
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Arthritis Res Ther 10:R37. 2008
    ..The objective of the present study was to investigate the role of the stromal cell-derived factor 1 (SDF-1)/CXCR4 axis in TNF-induced mobilization of osteoclast precursors (OCPs) from bone marrow...
  4. pmc Increased lymphangiogenesis in joints of mice with inflammatory arthritis
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Arthritis Res Ther 9:R118. 2007
    ..The lymphatic system may play an important role in the pathogenesis of inflammatory arthritis...
  5. ncbi request reprint TNF-alpha and pathologic bone resorption
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Keio J Med 54:127-31. 2005
    ..Here we review our current understanding of the mechanisms whereby TNFa increases osteoclastogenesis in vitro and in vivo...
  6. ncbi request reprint New roles for osteoclasts in bone
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Ann N Y Acad Sci 1116:245-54. 2007
    ..In this article, we review these findings, which support new roles for osteoclasts and OCPs in the growing field of osteoimmunology and in common pathologic conditions affecting bones and joints...
  7. ncbi request reprint Roles for NF-kappaB and c-Fos in osteoclasts
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    J Bone Miner Metab 23:11-5. 2005
    ....
  8. ncbi request reprint The RANKL/RANK/OPG pathway
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Curr Osteoporos Rep 5:98-104. 2007
    ..This article reviews the roles of the RANKL/RANK/OPG system in bone and other tissues...
  9. ncbi request reprint Osteoclast precursors: cytokine-stimulated immunomodulators of inflammatory bone disease
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA
    Curr Opin Rheumatol 18:427-32. 2006
    ..We review the regulation of OCP formation and differentiation, and propose that they are not only sources of bone-resorbing osteoclasts, but also of immune cells that influence the progression of inflammatory bone diseases...
  10. ncbi request reprint Future anti-catabolic therapeutic targets in bone disease
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY, 14642, USA
    Ann N Y Acad Sci 1068:447-57. 2006
    ....
  11. pmc Functions of RANKL/RANK/OPG in bone modeling and remodeling
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Arch Biochem Biophys 473:139-46. 2008
    ..Thus, the relative concentration of RANKL and OPG in bone is a major determinant of bone mass and strength. Here, we review our current understanding of the role of the RANKL/RANK/OPG system in bone modeling and remodeling...
  12. doi request reprint Bruton and Tec: new links in osteoimmunology
    Brendan F Boyce
    University of Rochester Medical Center, University of Rochester, Rochester, NY 14534, USA
    Cell Metab 7:283-5. 2008
    ..A new study by Shinohara et al. (2008) shows that protein phosphorylation by the tyrosine kinases Bruton and Tec links immunity and bone as well as two signaling pathways in precursors of osteoclasts, the cells that degrade bone...
  13. pmc Functions of nuclear factor kappaB in bone
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA
    Ann N Y Acad Sci 1192:367-75. 2010
    ..NF-kappaB inhibitors have been developed, but none have made it to clinical trials for the treatment of common bone diseases. Here we review the roles for NF-kappaB in bone and in common bone diseases...
  14. pmc Osteoclasts have multiple roles in bone in addition to bone resorption
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Crit Rev Eukaryot Gene Expr 19:171-80. 2009
    ..Here, we review these findings, which define new roles for osteoclasts and OCPs in the growing field of osteoimmunology and in common pathologic conditions in which bone resorption is increased...
  15. pmc Biology of RANK, RANKL, and osteoprotegerin
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    Arthritis Res Ther 9:S1. 2007
    ..Here we review our current understanding of the role of the RANKL/RANK/OPG system in bone and other tissues...
  16. doi request reprint Sphingosine-1 phosphate: a new player in osteoimmunology
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA
    Dev Cell 16:323-4. 2009
    ..shows that sphingosine-1 phosphate in blood attracts osteoclast precursors into the bloodstream to keep them away from bone surfaces. These findings point to a novel mechanism to inhibit bone degradation and prevent bone loss...
  17. ncbi request reprint SRC inhibitors in metastatic bone disease
    Brendan F Boyce
    University of Rochester Medical Center, Rochester, New York 14642, USA
    Clin Cancer Res 12:6291s-6295s. 2006
    ....
  18. ncbi request reprint NF-kappaB p50 and p52 expression is not required for RANK-expressing osteoclast progenitor formation but is essential for RANK- and cytokine-mediated osteoclastogenesis
    Lianping Xing
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, New York 14642, USA
    J Bone Miner Res 17:1200-10. 2002
    ....
  19. ncbi request reprint Expression of either NF-kappaB p50 or p52 in osteoclast precursors is required for IL-1-induced bone resorption
    Lianping Xing
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Bone Miner Res 18:260-9. 2003
    ..Thus, expression of either NF-kappaB p50 or p52 is required in osteoclasts and their precursors, rather than osteoblasts, for IL-1-mediated bone resorption...
  20. ncbi request reprint RANK signaling is not required for TNFalpha-mediated increase in CD11(hi) osteoclast precursors but is essential for mature osteoclast formation in TNFalpha-mediated inflammatory arthritis
    Ping Li
    Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Bone Miner Res 19:207-13. 2004
    ..RANK signaling is not required for the TNFalpha-stimulated increase in CD11b(hi) osteoclast precursors but is essential for mature osteoclast formation...
  21. ncbi request reprint In vivo RANK signaling blockade using the receptor activator of NF-kappaB:Fc effectively prevents and ameliorates wear debris-induced osteolysis via osteoclast depletion without inhibiting osteogenesis
    Lisa M Childs
    Department of Microbiology and Immunology, University of Rochester Medical Center, New York 14642, USA
    J Bone Miner Res 17:192-9. 2002
    ..These studies indicate that osteoclast depletion via RANK blockade is an effective method to prevent and reverse wear debris-induced osteolysis without jeopardizing osteogenesis...
  22. ncbi request reprint NF-kappaB p50 and p52 regulate receptor activator of NF-kappaB ligand (RANKL) and tumor necrosis factor-induced osteoclast precursor differentiation by activating c-Fos and NFATc1
    Teruhito Yamashita
    Department of Pathology and Laboratory Medicine and Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 282:18245-53. 2007
    ..Inhibition of NF-kappaB should prevent RANKL- and TNF-induced bone resorption...
  23. pmc NF-kappaB p100 limits TNF-induced bone resorption in mice by a TRAF3-dependent mechanism
    Zhenqiang Yao
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    J Clin Invest 119:3024-34. 2009
    ..These findings suggest that upregulation of TRAF3 or NF-kappaB p100 expression or inhibition of NF-kappaB p100 degradation in OCPs could limit bone destruction and inflammation-induced bone loss in common bone diseases...
  24. pmc Osteoclast precursor interaction with bone matrix induces osteoclast formation directly by an interleukin-1-mediated autocrine mechanism
    Zhenqiang Yao
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Biol Chem 283:9917-24. 2008
    ..TNF could induce c-Fos expression in OCPs at sites of inflammation in bone to promote this autocrine mechanism and thus amplify bone loss...
  25. ncbi request reprint Tumor necrosis factor-alpha increases circulating osteoclast precursor numbers by promoting their proliferation and differentiation in the bone marrow through up-regulation of c-Fms expression
    Zhenqiang Yao
    Department of Pathology, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 281:11846-55. 2006
    ..Therefore, the first step of TNF-induced osteoclastogenesis is at the level of OCP genesis in the bone marrow, which represents another layer of regulation to control erosive disease...
  26. pmc Tumor necrosis factor promotes Runx2 degradation through up-regulation of Smurf1 and Smurf2 in osteoblasts
    Hiroyuki Kaneki
    Department of Pathology and Laboratory Medicine, University of Rochester, School of Medicine and Dentistry, NY 14642, USA
    J Biol Chem 281:4326-33. 2006
    ..We propose that one of the mechanisms by which TNF inhibits bone formation in inflammatory bone disorders is by promoting Runx2 proteasomal degradation through up-regulation of Smurf1 and Smurf2 expression...
  27. pmc Longitudinal assessment of synovial, lymph node, and bone volumes in inflammatory arthritis in mice by in vivo magnetic resonance imaging and microfocal computed tomography
    Steven T Proulx
    Center for Musculoskeletal Research, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Arthritis Rheum 56:4024-37. 2007
    ....
  28. pmc Osteoprotegerin, the bone protector, is a surprising target for beta-catenin signaling
    Brendan F Boyce
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    Cell Metab 2:344-5. 2005
  29. ncbi request reprint Osteoclast precursors, RANKL/RANK, and immunology
    Lianping Xing
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Immunol Rev 208:19-29. 2005
    ..Disruption of this cycle could provide a new strategy for the development of drugs to treat inflammatory arthritis and other disorders associated with elevated OCP/myeloid progenitors...
  30. pmc VEGF-C, a lymphatic growth factor, is a RANKL target gene in osteoclasts that enhances osteoclastic bone resorption through an autocrine mechanism
    Qian Zhang
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:13491-9. 2008
    ....
  31. pmc The role of bone marrow edema and lymphangiogenesis in inflammatory-erosive arthritis
    Edward M Schwarz
    The Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York 14642, USA
    Adv Exp Med Biol 658:1-10. 2010
    ....
  32. pmc Remodeling of cortical bone allografts mediated by adherent rAAV-RANKL and VEGF gene therapy
    Hiromu Ito
    The Center for Musculoskeletal Research, University of Rochester, 601 Elmwood Avenue, Box 665, Rochester, New York 14642, USA
    Nat Med 11:291-7. 2005
    ..In conclusion, we find that RANKL and VEGF are necessary and sufficient for efficient autograft remodeling and can be transferred using rAAV to revitalize structural allografts...
  33. ncbi request reprint MRI and quantification of draining lymph node function in inflammatory arthritis
    Steven T Proulx
    The Center for Musculoskeletal Research, University of Rochester, Rochester, NY 14642, USA
    Ann N Y Acad Sci 1117:106-23. 2007
    ..63, P = 0.01) between LNcap and synovial volume. TNF-Tg mice with a lower LNcap display an accelerated progression of arthritis. These results indicate a protective function of enhanced lymphatic drainage in inflammatory arthritis...
  34. ncbi request reprint Autoimmunity and bone
    Edward M Schwarz
    Department of Orthopaedics, University of Rochester Medical Center, 601 Elmwood Avenue, Box 665, Rochester, NY 14642, USA
    Ann N Y Acad Sci 1068:275-83. 2006
    ..Thus, systemic factors produced by autoimmunity have a dramatic impact on active myelopoiesis and bone homeostasis...
  35. ncbi request reprint Regulation of apoptosis in osteoclasts and osteoblastic cells
    Lianping Xing
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, NY, USA
    Biochem Biophys Res Commun 328:709-20. 2005
    ..Understanding the mechanisms and regulation of bone cell apoptosis will enhance our knowledge of bone cell function and help us to develop better therapeutics for the management of osteoporosis and other bone diseases...
  36. pmc Ubiquitin ligase Smurf1 mediates tumor necrosis factor-induced systemic bone loss by promoting proteasomal degradation of bone morphogenetic signaling proteins
    Ruolin Guo
    Department of Pathology and Laboratory Medicine, and Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Biol Chem 283:23084-92. 2008
    ..Inhibition of ubiquitin-mediated Smad1 and Runx2 degradation in osteoblasts could help to treat inflammation-induced osteoporosis...
  37. ncbi request reprint Systemic tumor necrosis factor alpha mediates an increase in peripheral CD11bhigh osteoclast precursors in tumor necrosis factor alpha-transgenic mice
    Ping Li
    University of Rochester Medical Center, Rochester, New York 14642, USA
    Arthritis Rheum 50:265-76. 2004
    ..To investigate the mechanisms whereby tumor necrosis factor alpha (TNFalpha) increases osteoclastogenesis in vivo...
  38. pmc Reduced COX-2 expression in aged mice is associated with impaired fracture healing
    Amish A Naik
    The Center for Musculoskeletal Research, University of Rochester, Rochester, New York 14642, USA
    J Bone Miner Res 24:251-64. 2009
    ..The findings suggest that COX-2/EP4 agonists may compensate for deficient molecular signals that result in the reduced fracture healing associated with aging...
  39. pmc Murine and chicken chondrocytes regulate osteoclastogenesis by producing RANKL in response to BMP2
    Michihiko Usui
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Bone Miner Res 23:314-25. 2008
    ..We report that hypertrophic chondrocytes induce osteoclast formation through RANKL production stimulated by BMP2 and Runx2/Smad1 and thus they may regulate resorption of calcified matrix by osteoclasts at growth plates...
  40. pmc Generation and characterization of androgen receptor knockout (ARKO) mice: an in vivo model for the study of androgen functions in selective tissues
    Shuyuan Yeh
    Departments of Urology and Pathology, George H Whipple Lab for Cancer Research, University of Rochester, Rochester, NY 14642, USA
    Proc Natl Acad Sci U S A 99:13498-503. 2002
    ..The cre-lox ARKO mouse provides a much-needed in vivo animal model to study androgen functions in the selective androgen target tissues in female or male mice...
  41. pmc Axin2 controls bone remodeling through the beta-catenin-BMP signaling pathway in adult mice
    Ying Yan
    Department of Orthopaedics, Center for Musculoskeletal Research, University of Rochester School of Medicine, Rochester, NY 14642, USA
    J Cell Sci 122:3566-78. 2009
    ..Taken together, our findings demonstrate that Axin2 is a key negative regulator in bone remodeling in adult mice and regulates osteoblast differentiation through the beta-catenin-BMP2/4-Osx signaling pathway in osteoblasts...
  42. pmc The ubiquitin E3 ligase WWP1 decreases CXCL12-mediated MDA231 breast cancer cell migration and bone metastasis
    Kristina Subik
    Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
    Bone 50:813-23. 2012
    ....
  43. pmc Inhibition of beta-catenin signaling causes defects in postnatal cartilage development
    Mo Chen
    Department of Orthopaedics, Center for Musculoskeletal Research, University of Rochester School of Medicine, Rochester, NY 14642, USA
    J Cell Sci 121:1455-65. 2008
    ..Altogether the findings confirm a crucial role for Wnt/beta-catenin in postnatal growth...
  44. pmc Elucidating bone marrow edema and myelopoiesis in murine arthritis using contrast-enhanced magnetic resonance imaging
    Steven T Proulx
    University of Rochester, Rochester, New York 14642, USA
    Arthritis Rheum 58:2019-29. 2008
    ..In this study, MRI of murine arthritis was used to elucidate its cellular composition and vascular involvement...
  45. pmc Lead exposure inhibits fracture healing and is associated with increased chondrogenesis, delay in cartilage mineralization, and a decrease in osteoprogenitor frequency
    Jonathan J Carmouche
    Center for Musculoskeletal Research, University of Rochester Medical Center, University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642, USA
    Environ Health Perspect 113:749-55. 2005
    ..We conclude that Pb delays fracture healing at environmentally relevant doses and induces fibrous nonunions at higher doses by inhibiting the progression of endochondral ossification...
  46. ncbi request reprint Malignant autosomal recessive osteopetrosis caused by spontaneous mutation of murine Rank
    Raj P Kapur
    Department of Pathology, Children s Hospital and Regional Medical Center, University of Washington, Seattle, Washington, USA
    J Bone Miner Res 19:1689-97. 2004
    ..The phenotype, including a block in RANKL-dependent osteoclast differentiation and lymph node agenesis, copies that of Rank(-/-) mice, which have been produced by targeted recombination...
  47. ncbi request reprint NF-kappaB specifically activates BMP-2 gene expression in growth plate chondrocytes in vivo and in a chondrocyte cell line in vitro
    Jian Q Feng
    Department of Oral Biology, School of Dentistry, University of Missouri, Kansas City, Missouri 64108, USA
    J Biol Chem 278:29130-5. 2003
    ..Therefore, in postnatal growth plate chondrocytes, expression of BMP-2 is regulated by NF-kappaB, which may play an important role in chondrogenesis...
  48. pmc Dimorphic effects of Notch signaling in bone homeostasis
    Feyza Engin
    Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 7703, USA
    Nat Med 14:299-305. 2008
    ..Together, these findings highlight the potential dimorphic effects of Notch signaling in bone homeostasis and may provide direction for novel therapeutic applications...
  49. ncbi request reprint Osteoclasts, no longer osteoblast slaves
    Brendan F Boyce
    Nat Med 12:1356-8. 2006
  50. ncbi request reprint CRTAP is required for prolyl 3- hydroxylation and mutations cause recessive osteogenesis imperfecta
    Roy Morello
    Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA
    Cell 127:291-304. 2006
    ..In humans, CRTAP mutations are associated with the clinical spectrum of recessive osteogenesis imperfecta, including the type II and VII forms. Hence, dysregulation of prolyl 3-hydroxylation is a mechanism for connective tissue disease...
  51. ncbi request reprint Bad bones, grey hair, one mutation
    Brendan F Boyce
    Nat Med 9:395-6. 2003
  52. pmc Advances in treating metastatic bone cancer: summary statement for the First Cambridge Conference
    Allan Lipton
    Milton S Hershey Medical Center, Penn State University College of Medicine, Hershey, Pennsylvania 17033 0850, USA, and Department of Oncology, Norwegian Radium Hospital, Oslo, Norway
    Clin Cancer Res 12:6209s-6212s. 2006
    ..The conclusions reached during the 2-day meeting are summarized in this article and presented in more detail in the individual articles and accompanying discussion sessions that comprise the conference proceedings...

Research Grants13

  1. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 1999
    ..abstract_text> ..
  2. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2009
    ....
  3. 2007 Bones and Teeth Gordon Research Conference
    BRENDAN BOYCE; Fiscal Year: 2007
    ..The format and atmosphere that characterizes the Gordon Research Conferences will foster the free exchange of ideas and discussing of future directions in the study and treatment of skeletal tissues. ..
  4. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2007
    ..Ultimately they should lead to the development of specific therapeutic agents to prevent and treat common bone diseases associated with increased osteoclast activity. ..
  5. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2006
    ..Ultimately they should lead to the development of specific therapeutic agents to prevent and treat common bone diseases associated with increased osteoclast activity. ..
  6. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2005
    ..Ultimately they should lead to the development of specific therapeutic agents to prevent and treat common bone diseases associated with increased osteoclast activity. ..
  7. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2004
    ..Ultimately they should lead to the development of specific therapeutic agents to prevent and treat common bone diseases associated with increased osteoclast activity. ..
  8. RANK/NF-KappaB signaling in chondrogenesis
    BRENDAN BOYCE; Fiscal Year: 2003
    ....
  9. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2002
    ..abstract_text> ..
  10. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2001
    ..abstract_text> ..
  11. STUDIES OF THE FATE OF THE OSTEOCLAST
    BRENDAN BOYCE; Fiscal Year: 2000
    ..abstract_text> ..
  12. STUDIES OF THE FATE OF THE OSTEOCLAST
    Brendan F Boyce; Fiscal Year: 2010
    ....