Devin S Gary

Summary

Affiliation: Kennedy Krieger Institute
Country: USA

Publications

  1. ncbi request reprint Restoring function after spinal cord injury: promoting spontaneous regeneration with stem cells and activity-based therapies
    Visar Belegu
    The International Center for Spinal Cord Injury, Kennedy Krieger Institute, Department of Neurology, Johns Hopkins University School of Medicine, 707 North Broadway, Room 518, Baltimore, MD 21205, USA
    Neurosurg Clin N Am 18:143-68, xi. 2007
  2. doi request reprint Electrical stimulation promotes the survival of oligodendrocytes in mixed cortical cultures
    Devin S Gary
    The International Center for Spinal Cord Injury, Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, USA
    J Neurosci Res 90:72-83. 2012
  3. ncbi request reprint Investigation of RNA interference to suppress expression of full-length and fragment human huntingtin
    Devin S Gary
    Department of Pathology, Division of Neuropathology International Center for Spinal Cord Injury, Kennedy Krieger Institute, Johns Hopkins University, Baltimore, Maryland 21205, USA
    Neuromolecular Med 9:145-55. 2007
  4. pmc Functional electrical stimulation helps replenish progenitor cells in the injured spinal cord of adult rats
    Daniel Becker
    International Center, for Spinal Cord Injury, Hugo Moser Research Institute, Department of Neurology, Johns Hopkins School of Medicine and Kennedy Krieger Institute, Baltimore, MD 21205, USA
    Exp Neurol 222:211-8. 2010
  5. ncbi request reprint Suppression of calcium release from inositol 1,4,5-trisphosphate-sensitive stores mediates the anti-apoptotic function of nuclear factor-kappaB
    Simonetta Camandola
    Laboratory of Neurosciences, National Institute on Aging NIH, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 280:22287-96. 2005
  6. ncbi request reprint Essential role for integrin linked kinase in Akt-mediated integrin survival signaling in hippocampal neurons
    Devin S Gary
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 84:878-90. 2003
  7. ncbi request reprint PTEN regulates Akt kinase activity in hippocampal neurons and increases their sensitivity to glutamate and apoptosis
    Devin S Gary
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 2:261-9. 2002
  8. doi request reprint Neural stem cells reduce brain injury after unilateral carotid ligation
    Anne M Comi
    Division of Neurology and Developmental Medicine, Kennedy Krieger Institute, and Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    Pediatr Neurol 38:86-92. 2008
  9. ncbi request reprint Neuroprotective and neurorestorative signal transduction mechanisms in brain aging: modification by genes, diet and behavior
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurobiol Aging 23:695-705. 2002
  10. ncbi request reprint Involvement of Gadd153 in the pathogenic action of presenilin-1 mutations
    Ollivier Milhavet
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 83:673-81. 2002

Detail Information

Publications14

  1. ncbi request reprint Restoring function after spinal cord injury: promoting spontaneous regeneration with stem cells and activity-based therapies
    Visar Belegu
    The International Center for Spinal Cord Injury, Kennedy Krieger Institute, Department of Neurology, Johns Hopkins University School of Medicine, 707 North Broadway, Room 518, Baltimore, MD 21205, USA
    Neurosurg Clin N Am 18:143-68, xi. 2007
    ....
  2. doi request reprint Electrical stimulation promotes the survival of oligodendrocytes in mixed cortical cultures
    Devin S Gary
    The International Center for Spinal Cord Injury, Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, USA
    J Neurosci Res 90:72-83. 2012
    ..This report suggests that patterned neuronal activity could repress delayed progression of white matter injury and promote CNS repair in neurological conditions that involve white matter damage...
  3. ncbi request reprint Investigation of RNA interference to suppress expression of full-length and fragment human huntingtin
    Devin S Gary
    Department of Pathology, Division of Neuropathology International Center for Spinal Cord Injury, Kennedy Krieger Institute, Johns Hopkins University, Baltimore, Maryland 21205, USA
    Neuromolecular Med 9:145-55. 2007
    ....
  4. pmc Functional electrical stimulation helps replenish progenitor cells in the injured spinal cord of adult rats
    Daniel Becker
    International Center, for Spinal Cord Injury, Hugo Moser Research Institute, Department of Neurology, Johns Hopkins School of Medicine and Kennedy Krieger Institute, Baltimore, MD 21205, USA
    Exp Neurol 222:211-8. 2010
    ..In uninjured rats, FES had no effect on cell birth/survival. This report suggests that controlled electrical activation of the CNS may enhance spontaneous regeneration after neurological injuries...
  5. ncbi request reprint Suppression of calcium release from inositol 1,4,5-trisphosphate-sensitive stores mediates the anti-apoptotic function of nuclear factor-kappaB
    Simonetta Camandola
    Laboratory of Neurosciences, National Institute on Aging NIH, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 280:22287-96. 2005
    ..Overexpression of Bcl-2 normalizes ER calcium homeostasis and prevents calcium-mediated apoptosis in RelA-deficient cells. These findings establish an ER calcium channel as a pivotal target for NF-kappaB-mediated cell survival signaling...
  6. ncbi request reprint Essential role for integrin linked kinase in Akt-mediated integrin survival signaling in hippocampal neurons
    Devin S Gary
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 84:878-90. 2003
    ..Activation of ILK and Akt were also required for neuroprotection by substrate-associated laminin. These results establish a novel pathway that signals cell survival in neurons in response to integrin receptor activation...
  7. ncbi request reprint PTEN regulates Akt kinase activity in hippocampal neurons and increases their sensitivity to glutamate and apoptosis
    Devin S Gary
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 2:261-9. 2002
    ..The ability of PTEN to modify neuronal sensitivity to glutamate also suggests possible roles for PTEN in regulating developmental and synaptic plasticity...
  8. doi request reprint Neural stem cells reduce brain injury after unilateral carotid ligation
    Anne M Comi
    Division of Neurology and Developmental Medicine, Kennedy Krieger Institute, and Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    Pediatr Neurol 38:86-92. 2008
    ..Neural stem cells have the potential to ameliorate ischemic injury in the immature brain, although tumor development is a serious concern...
  9. ncbi request reprint Neuroprotective and neurorestorative signal transduction mechanisms in brain aging: modification by genes, diet and behavior
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurobiol Aging 23:695-705. 2002
    ..The recent application of modem methods of molecular and cellular biology to the problem of brain aging is revealing a remarkable capacity within brain cells for adaptation to aging and resistance to disease...
  10. ncbi request reprint Involvement of Gadd153 in the pathogenic action of presenilin-1 mutations
    Ollivier Milhavet
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 83:673-81. 2002
    ..An abnormality in the translational regulation of Gadd153 may sensitize cells to the detrimental effects of ER stress and contribute to the pathogenic actions of PS1 mutations in FAD...
  11. ncbi request reprint RNA interference in biology and medicine
    Ollivier Milhavet
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Pharmacol Rev 55:629-48. 2003
    ..Pharmacologists have long dreamed of the ability to selectively antagonize or eliminate the function of individual proteins--RNAi technology may eventually make that dream a reality...
  12. doi request reprint Chondroitin sulfate proteoglycans inhibit oligodendrocyte myelination through PTPσ
    James C Pendleton
    International Center for Spinal Cord Injury, Hugo W Moser Research Institute at Kennedy Krieger, USA Johns Hopkins University School of Medicine, Department of Pathology, USA
    Exp Neurol 247:113-21. 2013
    ..The identification of PTPσ as a receptor for CSPGs, and the participation of ROCK downstream of CSPG exposure, reveal potential therapeutic targets to enhance white matter repair in the damaged CNS. ..
  13. ncbi request reprint Matrix metalloproteinase-1 activates a pertussis toxin-sensitive signaling pathway that stimulates the release of matrix metalloproteinase-9
    Katherine Conant
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Neurochem 82:885-93. 2002
    ..Together, these results suggest that MMP-1 signals through a pertussis toxin-sensitive G protein-coupled receptor...
  14. ncbi request reprint Olfactory bulbectomy protects hippocampal pyramidal neurons against excitotoxic death
    Devin S Gary
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Exp Neurol 176:266-8. 2002
    ..These findings provide the first evidence that olfactory input affects the vulnerability of neurons to excitotoxic death...