Ernesto Canalis

Summary

Affiliation: University of Connecticut Health Center
Country: USA

Publications

  1. pmc Hajdu-Cheney Syndrome, a Disease Associated with NOTCH2 Mutations
    Ernesto Canalis
    Departments of Orthopaedic Surgery and Medicine, and The UConn Musculoskeletal Institute, UConn Health, Farmington, CT, 06030 5456, USA
    Curr Osteoporos Rep 14:126-31. 2016
  2. pmc Effects of Sex and Notch Signaling on the Osteocyte Cell Pool
    Ernesto Canalis
    Department of Orthopaedic Surgery, UConn Musculoskeletal Institute, UConn Health, Farmington, Connecticut
    J Cell Physiol 232:363-370. 2017
  3. pmc Hajdu Cheney Mouse Mutants Exhibit Osteopenia, Increased Osteoclastogenesis, and Bone Resorption
    Ernesto Canalis
    From the Departments of Orthopaedic Surgery, Medicine
    J Biol Chem 291:1538-51. 2016
  4. pmc Canonical Notch activation in osteocytes causes osteopetrosis
    Ernesto Canalis
    Department of Orthopedic Surgery and the University of Connecticut Musculoskeletal Institute, Farmington, Connecticut and Department of Medicine, University of Connecticut Health, Farmington, Connecticut
    Am J Physiol Endocrinol Metab 310:E171-82. 2016
  5. pmc Hajdu-Cheney syndrome: a review
    Ernesto Canalis
    Departments of Orthopaedic Surgery and Medicine, UConn Health, 263 Farmington Avenue, Farmington, CT 06030, USA
    Orphanet J Rare Dis 9:200. 2014
  6. pmc The Dmp1-SOST Transgene Interacts With and Downregulates the Dmp1-Cre Transgene and the Rosa(Notch) Allele
    Stefano Zanotti
    Departments of Orthopaedic Surgery and Medicine, and The UConn Musculoskeletal Institute, UConn Health, Farmington, 06030, Connecticut
    J Cell Biochem 117:1222-32. 2016
  7. pmc CCAAT/Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia
    Renata C Pereira
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, USA
    Bone 40:619-26. 2007
  8. pmc Connective tissue growth factor is a target of notch signaling in cells of the osteoblastic lineage
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, 06105 The University of Connecticut School of Medicine, Farmington, CT, 06030 Electronic address
    Bone 64:273-80. 2014
  9. pmc Connective tissue growth factor (CTGF) transactivates nuclear factor of activated T-cells (NFAT) in cells of the osteoblastic lineage
    Anna Smerdel-Ramoya
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut, USA
    J Cell Biochem 110:477-83. 2010
  10. pmc Col3.6-HSD2 transgenic mice: a glucocorticoid loss-of-function model spanning early and late osteoblast differentiation
    Maobin Yang
    Department of Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
    Bone 47:573-82. 2010

Collaborators

Detail Information

Publications18

  1. pmc Hajdu-Cheney Syndrome, a Disease Associated with NOTCH2 Mutations
    Ernesto Canalis
    Departments of Orthopaedic Surgery and Medicine, and The UConn Musculoskeletal Institute, UConn Health, Farmington, CT, 06030 5456, USA
    Curr Osteoporos Rep 14:126-31. 2016
    ..In conclusion, HCS is a devastating disease associated with a gain-of-NOTCH2 function resulting in diverse clinical manifestations. ..
  2. pmc Effects of Sex and Notch Signaling on the Osteocyte Cell Pool
    Ernesto Canalis
    Department of Orthopaedic Surgery, UConn Musculoskeletal Institute, UConn Health, Farmington, Connecticut
    J Cell Physiol 232:363-370. 2017
    ..J. Cell. Physiol. 232: 363-370, 2017. © 2016 Wiley Periodicals, Inc...
  3. pmc Hajdu Cheney Mouse Mutants Exhibit Osteopenia, Increased Osteoclastogenesis, and Bone Resorption
    Ernesto Canalis
    From the Departments of Orthopaedic Surgery, Medicine
    J Biol Chem 291:1538-51. 2016
    ..These effects were suppressed by the γ-secretase inhibitor LY450139. In conclusion, Notch2(Q2319X) mice exhibit cancellous and cortical bone osteopenia, enhanced osteoclastogenesis, and increased bone resorption. ..
  4. pmc Canonical Notch activation in osteocytes causes osteopetrosis
    Ernesto Canalis
    Department of Orthopedic Surgery and the University of Connecticut Musculoskeletal Institute, Farmington, Connecticut and Department of Medicine, University of Connecticut Health, Farmington, Connecticut
    Am J Physiol Endocrinol Metab 310:E171-82. 2016
    ..In conclusion, Notch activation in osteocytes suppresses bone resorption and increases bone volume by utilization of canonical signals that also result in the inhibition of Sost and Dkk1 and upregulation of Wnt signaling. ..
  5. pmc Hajdu-Cheney syndrome: a review
    Ernesto Canalis
    Departments of Orthopaedic Surgery and Medicine, UConn Health, 263 Farmington Avenue, Farmington, CT 06030, USA
    Orphanet J Rare Dis 9:200. 2014
    ..In conclusion, Notch regulates skeletal development and bone remodeling, and gain-of-function mutations of NOTCH2 are associated with HCS. ..
  6. pmc The Dmp1-SOST Transgene Interacts With and Downregulates the Dmp1-Cre Transgene and the Rosa(Notch) Allele
    Stefano Zanotti
    Departments of Orthopaedic Surgery and Medicine, and The UConn Musculoskeletal Institute, UConn Health, Farmington, 06030, Connecticut
    J Cell Biochem 117:1222-32. 2016
    ..In conclusion, the Dmp1-SOST transgene suppresses the expression of the Dmp1-Cre transgene and of Rosa26...
  7. pmc CCAAT/Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia
    Renata C Pereira
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, USA
    Bone 40:619-26. 2007
    ..In conclusion, transgenic mice overexpressing CHOP in the bone microenvironment have impaired osteoblastic function leading to osteopenia...
  8. pmc Connective tissue growth factor is a target of notch signaling in cells of the osteoblastic lineage
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, 06105 The University of Connecticut School of Medicine, Farmington, CT, 06030 Electronic address
    Bone 64:273-80. 2014
    ..In conclusion, Ctgf is a target of Notch canonical signaling in osteoblasts, and may act in concert with Notch to regulate skeletal homeostasis. ..
  9. pmc Connective tissue growth factor (CTGF) transactivates nuclear factor of activated T-cells (NFAT) in cells of the osteoblastic lineage
    Anna Smerdel-Ramoya
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut, USA
    J Cell Biochem 110:477-83. 2010
    ..4 promoter, confirming the role of cGKII in the activation of NFAT by CTGF. In conclusion, CTGF enhances NFAT signaling through the induction of cGKII and the phosphorylation of GSK3beta...
  10. pmc Col3.6-HSD2 transgenic mice: a glucocorticoid loss-of-function model spanning early and late osteoblast differentiation
    Maobin Yang
    Department of Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
    Bone 47:573-82. 2010
    ..These data further strengthen the concept that endogenous glucocorticoid signaling is required for optimal bone mass acquisition and highlight the complexities of glucocorticoid signaling in bone cell lineages...
  11. ncbi request reprint Effects of activated T cells on osteoclastogenesis depend on how they are activated
    Nancy Wyzga
    Connecticut Children s Medical Center, Hartford, CT, USA
    Bone 35:614-20. 2004
    ..Both pro- and anti-resorptive properties have been described. We reasoned that this reported variability of the effects of T cells on osteoclast formation depends on how T cells are activated in vitro...
  12. pmc Notch1 and Notch2 expression in osteoblast precursors regulates femoral microarchitecture
    Stefano Zanotti
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT, USA University of Connecticut School of Medicine, Farmington, CT, USA
    Bone 62:22-8. 2014
    ..These effects were modest and more evident in 3 and 6 month old female than in male mice of the same age. In conclusion, Notch1 and Notch2 expression in osteoblast precursors regulates cancellous bone volume and microarchitecture...
  13. ncbi request reprint Mechanisms of glucocorticoid-induced osteoporosis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, and University of Connecticut School of Medicine, Farmington, Connecticut, USA
    Curr Opin Rheumatol 15:454-7. 2003
    ..Eventually, the inhibition of bone formation will cause a decrease in bone remodeling and a continued increased risk of fractures...
  14. pmc Nemo-like kinase regulates postnatal skeletal homeostasis
    Ernesto Canalis
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut The University of Connecticut School of Medicine, Farmington, Connecticut
    J Cell Physiol 229:1736-43. 2014
    ..In conclusion, when expressed in undifferentiated osteoblasts, Nlk is a negative regulator of skeletal homeostasis possibly by targeting signals that regulate osteoclastogenesis and bone resorption...
  15. pmc Notch Signaling and the Skeleton
    Stefano Zanotti
    Departments of Orthopaedic Surgery and Medicine and the UConn Musculoskeletal Institute, UConn Health, Farmington, Connecticut 06030
    Endocr Rev 37:223-53. 2016
    ..In conclusion, Notch plays a critical role in skeletal development and homeostasis, and serious skeletal disorders can be attributed to alterations in Notch signaling. ..
  16. pmc Sex and genetic factors determine osteoblastic differentiation potential of murine bone marrow stromal cells
    Stefano Zanotti
    Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut, United States of America University of Connecticut School of Medicine, University of Connecticut Health Center, Farmington, Connecticut, United States of America
    PLoS ONE 9:e86757. 2014
    ..In conclusion, osteoblastogenesis is sexually dimorphic and influenced by genetic factors. ..
  17. doi request reprint Hairy and Enhancer of Split-related with YRPW Motif-Like (HeyL) is Dispensable for Bone Remodeling in Mice
    Ernesto Canalis
    Departments of Orthopaedic Surgery and Medicine, and The UConn Musculoskeletal Institute, UConn Health, Farmington, CT, 06030
    J Cell Biochem . 2016
    ..In conclusion, HeyL null mice do not exhibit an obvious skeletal phenotype demonstrating that HeyL is dispensable for skeletal homeostasis. This article is protected by copyright. All rights reserved...
  18. pmc Activation of Nfatc2 in osteoblasts causes osteopenia
    Stefano Zanotti
    Departments of Orthopaedic Surgery and Medicine, UCONN Health Center, Farmington, Connecticut
    J Cell Physiol 230:1689-95. 2015
    ..In conclusion, Nfatc2 activation in osteoblasts inhibits bone formation and causes cancellous bone osteopenia...