Despina Sitara

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice
    Despina Sitara
    Department of Oral and Developmental Biology, The Forsyth Institute, Harvard School of Dental Medicine, 140 The Fenway, Boston, MA, 02115, USA
    Matrix Biol 23:421-32. 2004
  2. pmc Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, REB 303, 188 Longwood Ave, Boston, MA 02115, USA, and The Genetics Unit, Shriners Hospital, Montreal, Quebec, Canada
    Am J Pathol 169:2161-70. 2006
  3. pmc Genetic evidence of serum phosphate-independent functions of FGF-23 on bone
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts, United States of America
    PLoS Genet 4:e1000154. 2008
  4. ncbi request reprint Correlation among hyperphosphatemia, type II sodium phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA
    Ann N Y Acad Sci 1116:485-93. 2007
  5. pmc PTH ablation ameliorates the anomalies of Fgf23-deficient mice by suppressing the elevated vitamin D and calcium levels
    Quan Yuan
    Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room 303, 188 Longwood Avenue, Boston, Massachusetts 02115, USA
    Endocrinology 152:4053-61. 2011
  6. pmc Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process
    Mohammed S Razzaque
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA
    FASEB J 20:720-2. 2006
  7. pmc Zfp521 is a target gene and key effector of parathyroid hormone-related peptide signaling in growth plate chondrocytes
    Diego Correa
    Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA
    Dev Cell 19:533-46. 2010
  8. 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
  9. pmc The collection of NFATc1-dependent transcripts in the osteoclast includes numerous genes non-essential to physiologic bone resorption
    Julia F Charles
    Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Bone 51:902-12. 2012
  10. pmc Transcriptional regulation of bone and joint remodeling by NFAT
    Despina Sitara
    Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA 02115, USA
    Immunol Rev 233:286-300. 2010

Collaborators

Detail Information

Publications11

  1. pmc Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice
    Despina Sitara
    Department of Oral and Developmental Biology, The Forsyth Institute, Harvard School of Dental Medicine, 140 The Fenway, Boston, MA, 02115, USA
    Matrix Biol 23:421-32. 2004
    ....
  2. pmc Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, REB 303, 188 Longwood Ave, Boston, MA 02115, USA, and The Genetics Unit, Shriners Hospital, Montreal, Quebec, Canada
    Am J Pathol 169:2161-70. 2006
    ....
  3. pmc Genetic evidence of serum phosphate-independent functions of FGF-23 on bone
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts, United States of America
    PLoS Genet 4:e1000154. 2008
    ....
  4. ncbi request reprint Correlation among hyperphosphatemia, type II sodium phosphate transporter activity, and vitamin D metabolism in Fgf-23 null mice
    Despina Sitara
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA
    Ann N Y Acad Sci 1116:485-93. 2007
    ....
  5. pmc PTH ablation ameliorates the anomalies of Fgf23-deficient mice by suppressing the elevated vitamin D and calcium levels
    Quan Yuan
    Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room 303, 188 Longwood Avenue, Boston, Massachusetts 02115, USA
    Endocrinology 152:4053-61. 2011
    ..These results indicate that PTH is able to modulate the anomalies of Fgf23-/- mice by controlling serum 1,25(OH)2D and calcium levels...
  6. pmc Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process
    Mohammed S Razzaque
    Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA
    FASEB J 20:720-2. 2006
    ..Finally, our data support a new model of interactions among Fgf-23, vitamin D, and klotho, a gene described as being associated with premature aging process...
  7. pmc Zfp521 is a target gene and key effector of parathyroid hormone-related peptide signaling in growth plate chondrocytes
    Diego Correa
    Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA
    Dev Cell 19:533-46. 2010
    ..Thus, Zfp521 is an important PTHrP target gene that regulates growth plate chondrocyte proliferation and differentiation...
  8. 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...
  9. pmc The collection of NFATc1-dependent transcripts in the osteoclast includes numerous genes non-essential to physiologic bone resorption
    Julia F Charles
    Department of Medicine, Division of Rheumatology, Allergy and Immunology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Bone 51:902-12. 2012
    ..These data highlight the need for rigorous validation studies to complement expression profiling results before functional importance can be assigned to highly regulated genes in any biologic process...
  10. pmc Transcriptional regulation of bone and joint remodeling by NFAT
    Despina Sitara
    Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA 02115, USA
    Immunol Rev 233:286-300. 2010
    ..The goal of this article is to highlight the importance of tissue remodeling in musculoskeletal disease and situate NFAT-driven cellular responses within this context to inspire future research endeavors...
  11. pmc Biological activity of FGF-23 fragments
    Theresa J Berndt
    Department of Internal Medicine, Mayo Clinic College of Medicine, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN 55905, USA
    Pflugers Arch 454:615-23. 2007
    ..We conclude that carboxyl terminal fragments of FGF-23 are phosphaturic and that a short, 26-amino acid fragment of FGF-23 retains significant phosphaturic activity...