Elisa Greggio

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Kinase activity is required for the toxic effects of mutant LRRK2/dardarin
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892 3707, USA
    Neurobiol Dis 23:329-41. 2006
  2. pmc The Parkinson disease-associated leucine-rich repeat kinase 2 (LRRK2) is a dimer that undergoes intramolecular autophosphorylation
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, NIA, National Institutes of Health, Bethesda, MD 20892, USA
    J Biol Chem 283:16906-14. 2008
  3. ncbi request reprint Kinase signaling pathways as potential targets in the treatment of Parkinson's disease
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20982, USA
    Expert Rev Proteomics 4:783-92. 2007
  4. pmc The R1441C mutation of LRRK2 disrupts GTP hydrolysis
    Patrick A Lewis
    Laboratory of Neurogenetics, National Institute on Aging, 35 Convent Drive, Bethesda, MD 20892 3707, USA
    Biochem Biophys Res Commun 357:668-71. 2007
  5. ncbi request reprint Mutations in LRRK2/dardarin associated with Parkinson disease are more toxic than equivalent mutations in the homologous kinase LRRK1
    Elisa Greggio
    Cell Biology and Gene Expression Unit, National Institute on Aging, Bethesda, Maryland 20982 3707, USA
    J Neurochem 102:93-102. 2007
  6. pmc The Parkinson's disease associated LRRK2 exhibits weaker in vitro phosphorylation of 4E-BP compared to autophosphorylation
    Azad Kumar
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 5:e8730. 2010
  7. pmc The Parkinson's disease kinase LRRK2 autophosphorylates its GTPase domain at multiple sites
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892 3707, USA
    Biochem Biophys Res Commun 389:449-54. 2009
  8. pmc The chaperone activity of heat shock protein 90 is critical for maintaining the stability of leucine-rich repeat kinase 2
    Lizhen Wang
    Unit of Transgenesis, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland 20892, USA
    J Neurosci 28:3384-91. 2008
  9. pmc Formation of a stabilized cysteine sulfinic acid is critical for the mitochondrial function of the parkinsonism protein DJ-1
    Jeff Blackinton
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, NIA, National Institutes of Health, Bethesda, Maryland 20892 3707, USA
    J Biol Chem 284:6476-85. 2009
  10. pmc Analysis of IFT74 as a candidate gene for chromosome 9p-linked ALS-FTD
    Parastoo Momeni
    Laboratory of Neurogenetics, National Institute of Aging, NIH, Bethesda, MD, USA
    BMC Neurol 6:44. 2006

Detail Information

Publications12

  1. ncbi request reprint Kinase activity is required for the toxic effects of mutant LRRK2/dardarin
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892 3707, USA
    Neurobiol Dis 23:329-41. 2006
    ..We also show that dardarin protein is expressed within human midbrain neurons and that C-terminal epitopes are also found in some Lewy bodies...
  2. pmc The Parkinson disease-associated leucine-rich repeat kinase 2 (LRRK2) is a dimer that undergoes intramolecular autophosphorylation
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, NIA, National Institutes of Health, Bethesda, MD 20892, USA
    J Biol Chem 283:16906-14. 2008
    ..Finally, we demonstrate that LRRK2 undergoes intramolecular autophosphorylation. Together, these results provide insight into the mechanism and regulation of LRRK2 kinase activity...
  3. ncbi request reprint Kinase signaling pathways as potential targets in the treatment of Parkinson's disease
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20982, USA
    Expert Rev Proteomics 4:783-92. 2007
    ....
  4. pmc The R1441C mutation of LRRK2 disrupts GTP hydrolysis
    Patrick A Lewis
    Laboratory of Neurogenetics, National Institute on Aging, 35 Convent Drive, Bethesda, MD 20892 3707, USA
    Biochem Biophys Res Commun 357:668-71. 2007
    ..We show that LRRK2 immunoprecipitated from cells has a detectable GTPase activity that is disrupted by a familial mutation associated with PD located within the GTPase domain, R1441C...
  5. ncbi request reprint Mutations in LRRK2/dardarin associated with Parkinson disease are more toxic than equivalent mutations in the homologous kinase LRRK1
    Elisa Greggio
    Cell Biology and Gene Expression Unit, National Institute on Aging, Bethesda, Maryland 20982 3707, USA
    J Neurochem 102:93-102. 2007
    ..We show that mutations in dardarin are more prone to form inclusion bodies in transfected cells and are more toxic than equivalent mutations in LRRK1. This work suggests that dardarin/LRRK2 is inherently more damaging than LRRK1...
  6. pmc The Parkinson's disease associated LRRK2 exhibits weaker in vitro phosphorylation of 4E-BP compared to autophosphorylation
    Azad Kumar
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 5:e8730. 2010
    ..Overall, our results suggest that 4E-BP is a relatively poor direct substrate for LRRK2...
  7. pmc The Parkinson's disease kinase LRRK2 autophosphorylates its GTPase domain at multiple sites
    Elisa Greggio
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892 3707, USA
    Biochem Biophys Res Commun 389:449-54. 2009
    ..These data suggest that the kinase and GTPase activities of LRRK2 may exhibit complex autoregulatory interdependence...
  8. pmc The chaperone activity of heat shock protein 90 is critical for maintaining the stability of leucine-rich repeat kinase 2
    Lizhen Wang
    Unit of Transgenesis, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland 20892, USA
    J Neurosci 28:3384-91. 2008
    ..Therefore, inhibition of LRRK2 kinase activity can be achieved by blocking Hsp90-mediated chaperone activity and Hsp90 inhibitors may serve as potential anti-PD drugs...
  9. pmc Formation of a stabilized cysteine sulfinic acid is critical for the mitochondrial function of the parkinsonism protein DJ-1
    Jeff Blackinton
    Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, NIA, National Institutes of Health, Bethesda, Maryland 20892 3707, USA
    J Biol Chem 284:6476-85. 2009
    ..We therefore conclude that formation of Cys106-sulfinic acid is a key modification that regulates the protective function of DJ-1...
  10. pmc Analysis of IFT74 as a candidate gene for chromosome 9p-linked ALS-FTD
    Parastoo Momeni
    Laboratory of Neurogenetics, National Institute of Aging, NIH, Bethesda, MD, USA
    BMC Neurol 6:44. 2006
    ..A new locus for amyotrophic lateral sclerosis--frontotemporal dementia (ALS-FTD) has recently been ascribed to chromosome 9p...
  11. pmc Structure of the ROC domain from the Parkinson's disease-associated leucine-rich repeat kinase 2 reveals a dimeric GTPase
    Junpeng Deng
    Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, OK 74078, USA
    Proc Natl Acad Sci U S A 105:1499-504. 2008
    ..The structure of the LRRK2 ROC domain also represents a signature from a previously undescribed class of GTPases from complex proteins and results may provide a unique molecular target for therapeutics in PD...
  12. ncbi request reprint Tyrosinase exacerbates dopamine toxicity but is not genetically associated with Parkinson's disease
    Elisa Greggio
    Department of Biology, University of Padova, Padova, Italy
    J Neurochem 93:246-56. 2005
    ..This argues against a strong genetic association between tyrosinase and PD, although the observed contribution to cellular toxicity suggests that a biochemical association is likely...