Matthew B Greenblatt

Summary

Publications

  1. doi request reprint Mitogen-activated protein kinase pathways in osteoblasts
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115 email
    Annu Rev Cell Dev Biol 29:63-79. 2013
  2. pmc The immune pathogenesis of scleroderma: context is everything
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Curr Rheumatol Rep 15:297. 2013
  3. pmc The p38 MAPK pathway is essential for skeletogenesis and bone homeostasis in mice
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, and Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 120:2457-73. 2010
  4. pmc MLK3 regulates bone development downstream of the faciogenital dysplasia protein FGD1 in mice
    Weiguo Zou
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    J Clin Invest 121:4383-92. 2011
  5. pmc NFATc1 and NFATc2 repress spontaneous osteoarthritis
    Matthew B Greenblatt
    Department of Pathology, Division of Rheumatology, Allergy and Immunology, Department of Medicine, and Department of Orthopedics, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115
    Proc Natl Acad Sci U S A 110:19914-9. 2013
  6. pmc CHMP5 controls bone turnover rates by dampening NF-κB activity in osteoclasts
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115 Department of Medicine and Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065
    J Exp Med 212:1283-301. 2015
  7. pmc TAK1 mediates BMP signaling in cartilage
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    Ann N Y Acad Sci 1192:385-90. 2010
  8. pmc Administration of BMP2/7 in utero partially reverses Rubinstein-Taybi syndrome-like skeletal defects induced by Pdk1 or Cbp mutations in mice
    Jae Hyuck Shim
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    J Clin Invest 122:91-106. 2012
  9. pmc Interspecies comparison of human and murine scleroderma reveals IL-13 and CCL2 as disease subset-specific targets
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Am J Pathol 180:1080-94. 2012
  10. pmc p38α MAPK is required for tooth morphogenesis and enamel secretion
    Matthew B Greenblatt
    From the Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115
    J Biol Chem 290:284-95. 2015

Collaborators

Detail Information

Publications12

  1. doi request reprint Mitogen-activated protein kinase pathways in osteoblasts
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115 email
    Annu Rev Cell Dev Biol 29:63-79. 2013
    ....
  2. pmc The immune pathogenesis of scleroderma: context is everything
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Curr Rheumatol Rep 15:297. 2013
    ..These developments will help build a context for better understanding of previous observations and design of the next generation of studies that may eventually lead to effective treatment...
  3. pmc The p38 MAPK pathway is essential for skeletogenesis and bone homeostasis in mice
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, and Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 120:2457-73. 2010
    ..These results also suggest that selective p38beta agonists may represent attractive therapeutic agents to prevent bone loss associated with osteoporosis and aging...
  4. pmc MLK3 regulates bone development downstream of the faciogenital dysplasia protein FGD1 in mice
    Weiguo Zou
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    J Clin Invest 121:4383-92. 2011
    ..Thus, our results provide a putative biochemical mechanism for the skeletal defects in human FGDY and suggest that modulating MAPK signaling may benefit these patients...
  5. pmc NFATc1 and NFATc2 repress spontaneous osteoarthritis
    Matthew B Greenblatt
    Department of Pathology, Division of Rheumatology, Allergy and Immunology, Department of Medicine, and Department of Orthopedics, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115
    Proc Natl Acad Sci U S A 110:19914-9. 2013
    ..Furthermore, these findings indicate that NFATs are key suppressors of OA, and regulating NFATs or their transcriptional targets in chondrocytes may lead to novel disease-modifying OA therapies. ..
  6. pmc CHMP5 controls bone turnover rates by dampening NF-κB activity in osteoclasts
    Matthew B Greenblatt
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115 Department of Medicine and Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10065
    J Exp Med 212:1283-301. 2015
    ..Thus, CHMP5 tunes NF-κB signaling downstream of RANK in osteoclasts to dampen osteoclast differentiation, osteoblast coupling and bone turnover rates, and disruption of CHMP5 activity results in a PDB-like skeletal disorder. ..
  7. pmc TAK1 mediates BMP signaling in cartilage
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    Ann N Y Acad Sci 1192:385-90. 2010
    ..Biochemical analysis suggests that TAK1 can interact with Smad proteins and promote their activation through phosphorylation, revealing a previously unrecognized crosstalk between the MAPK and Smad arms of BMP signaling...
  8. pmc Administration of BMP2/7 in utero partially reverses Rubinstein-Taybi syndrome-like skeletal defects induced by Pdk1 or Cbp mutations in mice
    Jae Hyuck Shim
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA
    J Clin Invest 122:91-106. 2012
    ..These findings illustrate the in vivo function of the PDK1-AKT-CREB/CBP pathway in bone formation and provide proof of principle for in utero growth factor supplementation as a potential therapy for skeletal dysplasias...
  9. pmc Interspecies comparison of human and murine scleroderma reveals IL-13 and CCL2 as disease subset-specific targets
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Am J Pathol 180:1080-94. 2012
    ..This approach serves as a model for personalized translational medicine, in which well-characterized animal models are matched to molecularly stratified patient subsets...
  10. pmc p38α MAPK is required for tooth morphogenesis and enamel secretion
    Matthew B Greenblatt
    From the Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115
    J Biol Chem 290:284-95. 2015
    ..Thus, BMP-induced activation of the p38α MAPK pathway is critical for the morphogenesis of tooth cusps and the secretion of dental enamel. ..
  11. pmc Calcineurin regulates innate antifungal immunity in neutrophils
    Matthew B Greenblatt
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
    J Exp Med 207:923-31. 2010
    ....
  12. pmc TAK1 is an essential regulator of BMP signalling in cartilage
    Jae Hyuck Shim
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
    EMBO J 28:2028-41. 2009
    ..Our experiments reveal an essential role for TAK1 in the morphogenesis, growth, and maintenance of cartilage...