Piera Pasinelli

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. ncbi Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria
    Piera Pasinelli
    Day Laboratory for Neuromuscular Research, Department of Neurology, Harvard Medical School, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Neuron 43:19-30. 2004
  2. ncbi A caspase-3-cleaved fragment of the glial glutamate transporter EAAT2 is sumoylated and targeted to promyelocytic leukemia nuclear bodies in mutant SOD1-linked amyotrophic lateral sclerosis
    Stuart L Gibb
    Farber Institute for Neurosciences, Weinberg Unit for ALS Research, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, and Cecil B Day Laboratory for Neuromuscular Research, Massachusetts General Hospital, Charlestown 02129, USA
    J Biol Chem 282:32480-90. 2007
  3. ncbi Caspase-3 cleaves and inactivates the glutamate transporter EAAT2
    William Boston-Howes
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Biol Chem 281:14076-84. 2006
  4. ncbi Molecular biology of amyotrophic lateral sclerosis: insights from genetics
    Piera Pasinelli
    Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Room 3125, Building 114, 16th Street, Navy Yard, Charlestown, Massachusetts 02429, USA
    Nat Rev Neurosci 7:710-23. 2006
  5. ncbi RNA interference-mediated silencing of mutant superoxide dismutase rescues cyclosporin A-induced death in cultured neuroblastoma cells
    Michele M Maxwell
    Day Laboratory for Neuromuscular Research and High Throughput Screening Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 101:3178-83. 2004
  6. ncbi Inhibition of SOD1 expression by mitomycin C is a non-specific consequence of cellular toxicity
    Wendy J Broom
    Day Neuromuscular Research Laboratory, Massachusetts General Hospital, MGH East, 114 16th Street, Navy Yard, Charlestown, MA 02129, USA
    Neurosci Lett 393:184-8. 2006
  7. ncbi Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS
    Daryl A Bosco
    Department of Neurology, University of Massachusetts Medical Center, Worcester, Massachusetts, USA
    Nat Neurosci 13:1396-403. 2010
  8. ncbi Molecular signature of late-stage human ALS revealed by expression profiling of postmortem spinal cord gray matter
    Fernando Dangond
    Laboratory of Transcriptional and Immune Regulation, Center for Neurologic Diseases, Brigham and Women's Hospital, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Physiol Genomics 16:229-39. 2004
  9. ncbi Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice
    Shan Zhu
    Neuroapoptosis Laboratory, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:5909-12. 2004
  10. ncbi Nordihydroguaiaretic acid increases glutamate uptake in vitro and in vivo: therapeutic implications for amyotrophic lateral sclerosis
    William Boston-Howes
    Weinberg Unit for ALS Research, Farber Institute for the Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Exp Neurol 213:229-37. 2008

Collaborators

Detail Information

Publications10

  1. ncbi Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria
    Piera Pasinelli
    Day Laboratory for Neuromuscular Research, Department of Neurology, Harvard Medical School, Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Neuron 43:19-30. 2004
    ..These findings provide new insights into the anti-apoptotic function of SOD1 and suggest that entrapment of Bcl-2 by large SOD1 aggregates may deplete motor neurons of this anti-apoptotic protein...
  2. ncbi A caspase-3-cleaved fragment of the glial glutamate transporter EAAT2 is sumoylated and targeted to promyelocytic leukemia nuclear bodies in mutant SOD1-linked amyotrophic lateral sclerosis
    Stuart L Gibb
    Farber Institute for Neurosciences, Weinberg Unit for ALS Research, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, and Cecil B Day Laboratory for Neuromuscular Research, Massachusetts General Hospital, Charlestown 02129, USA
    J Biol Chem 282:32480-90. 2007
    ....
  3. ncbi Caspase-3 cleaves and inactivates the glutamate transporter EAAT2
    William Boston-Howes
    Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Biol Chem 281:14076-84. 2006
    ..Taken together, our findings suggest that caspase-3 cleavage of EAAT2 is one mechanism responsible for the impairment of glutamate uptake in mutant SOD1-linked ALS...
  4. ncbi Molecular biology of amyotrophic lateral sclerosis: insights from genetics
    Piera Pasinelli
    Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Room 3125, Building 114, 16th Street, Navy Yard, Charlestown, Massachusetts 02429, USA
    Nat Rev Neurosci 7:710-23. 2006
    ..Here, we present an overview of the mechanisms for motor neuron death and of the role of non-neuronal cells in ALS...
  5. ncbi RNA interference-mediated silencing of mutant superoxide dismutase rescues cyclosporin A-induced death in cultured neuroblastoma cells
    Michele M Maxwell
    Day Laboratory for Neuromuscular Research and High Throughput Screening Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 101:3178-83. 2004
    ..The present study further supports the therapeutic potential of RNAi-based methods for the treatment of inherited human diseases, including ALS...
  6. ncbi Inhibition of SOD1 expression by mitomycin C is a non-specific consequence of cellular toxicity
    Wendy J Broom
    Day Neuromuscular Research Laboratory, Massachusetts General Hospital, MGH East, 114 16th Street, Navy Yard, Charlestown, MA 02129, USA
    Neurosci Lett 393:184-8. 2006
    ..Our data indicate the apparent inhibition of SOD1 expression by MC is a non-specific consequence of MC-induced cellular toxicity...
  7. ncbi Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS
    Daryl A Bosco
    Department of Neurology, University of Massachusetts Medical Center, Worcester, Massachusetts, USA
    Nat Neurosci 13:1396-403. 2010
    ..Our findings suggest that wild-type SOD1 can be pathogenic in SALS and identify an SOD1-dependent pathogenic mechanism common to FALS and SALS...
  8. ncbi Molecular signature of late-stage human ALS revealed by expression profiling of postmortem spinal cord gray matter
    Fernando Dangond
    Laboratory of Transcriptional and Immune Regulation, Center for Neurologic Diseases, Brigham and Women's Hospital, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Physiol Genomics 16:229-39. 2004
    ..It is apparent from this study that DNA microarray analysis and appropriate bioinformatics can reveal distinct phenotypic changes that underlie the terminal stages of neurodegeneration in ALS...
  9. ncbi Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice
    Shan Zhu
    Neuroapoptosis Laboratory, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 24:5909-12. 2004
    ..Prophylactic creatine supplementation, similar to what is recommended for an agent such as aspirin, may be considered for patients in high stroke-risk categories...
  10. ncbi Nordihydroguaiaretic acid increases glutamate uptake in vitro and in vivo: therapeutic implications for amyotrophic lateral sclerosis
    William Boston-Howes
    Weinberg Unit for ALS Research, Farber Institute for the Neurosciences, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Exp Neurol 213:229-37. 2008
    ....