Paola Scaffidi

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc In vitro generation of human cells with cancer stem cell properties
    Paola Scaffidi
    National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nat Cell Biol 13:1051-61. 2011
  2. pmc Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing
    Paola Scaffidi
    National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nat Cell Biol 10:452-9. 2008
  3. pmc Lamin A-dependent nuclear defects in human aging
    Paola Scaffidi
    National Cancer Institute NCI, NIH, Bethesda, MD 20892, USA
    Science 312:1059-63. 2006
  4. pmc The cell nucleus and aging: tantalizing clues and hopeful promises
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS Biol 3:e395. 2005
  5. pmc Good news in the nuclear envelope: loss of lamin A might be a gain
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Invest 116:632-4. 2006
  6. pmc Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA
    Nat Med 11:440-5. 2005
  7. ncbi request reprint Genome instability in progeria: when repair gets old
    Tom Misteli
    Nat Med 11:718-9. 2005
  8. ncbi request reprint GR and HMGB1 interact only within chromatin and influence each other's residence time
    Alessandra Agresti
    San Raffaele Research Institute, Via Olgettina 58, 20132 Milan, Italy
    Mol Cell 18:109-21. 2005
  9. pmc Distinct structural and mechanical properties of the nuclear lamina in Hutchinson-Gilford progeria syndrome
    Kris Noel Dahl
    Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 103:10271-6. 2006
  10. pmc Global nature of dynamic protein-chromatin interactions in vivo: three-dimensional genome scanning and dynamic interaction networks of chromatin proteins
    Robert D Phair
    BioInformatics Services, Rockville, MD 20854, USA
    Mol Cell Biol 24:6393-402. 2004

Collaborators

Detail Information

Publications11

  1. pmc In vitro generation of human cells with cancer stem cell properties
    Paola Scaffidi
    National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nat Cell Biol 13:1051-61. 2011
    ..These findings establish an experimental system to characterize cellular and molecular properties of human CSCs and demonstrate that somatic cells have the potential to de-differentiate and acquire properties of CSCs...
  2. pmc Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing
    Paola Scaffidi
    National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nat Cell Biol 10:452-9. 2008
    ..Our results support a model in which accelerated ageing in HGPS patients, and possibly also physiological ageing, is the result of adult stem cell dysfunction and progressive deterioration of tissue functions...
  3. pmc Lamin A-dependent nuclear defects in human aging
    Paola Scaffidi
    National Cancer Institute NCI, NIH, Bethesda, MD 20892, USA
    Science 312:1059-63. 2006
    ..Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging...
  4. pmc The cell nucleus and aging: tantalizing clues and hopeful promises
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS Biol 3:e395. 2005
  5. pmc Good news in the nuclear envelope: loss of lamin A might be a gain
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Invest 116:632-4. 2006
    ..The good news is these findings open the door to a new strategy for the therapeutic treatment of diseases caused by mutations in lamin A, such as muscular dystrophies and some types of premature aging syndromes...
  6. pmc Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome
    Paola Scaffidi
    National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA
    Nat Med 11:440-5. 2005
    ..Our results establish proof of principle for the correction of the premature aging phenotype in individuals with HGPS...
  7. ncbi request reprint Genome instability in progeria: when repair gets old
    Tom Misteli
    Nat Med 11:718-9. 2005
  8. ncbi request reprint GR and HMGB1 interact only within chromatin and influence each other's residence time
    Alessandra Agresti
    San Raffaele Research Institute, Via Olgettina 58, 20132 Milan, Italy
    Mol Cell 18:109-21. 2005
    ..We propose that kinetic cooperativity among transcription factors in chromatin binding may be a common feature in transcription and DNA transactions...
  9. pmc Distinct structural and mechanical properties of the nuclear lamina in Hutchinson-Gilford progeria syndrome
    Kris Noel Dahl
    Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 103:10271-6. 2006
    ....
  10. pmc Global nature of dynamic protein-chromatin interactions in vivo: three-dimensional genome scanning and dynamic interaction networks of chromatin proteins
    Robert D Phair
    BioInformatics Services, Rockville, MD 20854, USA
    Mol Cell Biol 24:6393-402. 2004
    ..We suggest that these properties are crucial for generating high plasticity in genome expression...
  11. pmc Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion
    Tiziana Bonaldi
    DIBIT, San Raffaele Scientific Institute, San Raffaele University, Via Olgettina 58, 20132 Milan, Italy
    EMBO J 22:5551-60. 2003
    ..Cytosolic HMGB1 is then concentrated by default into secretory lysosomes, and secreted when monocytic cells receive an appropriate second signal...