Research Topics
Genomes and GenesSpecies | Devin S GarySummaryAffiliation: Kennedy Krieger Institute Country: USA Publications
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Detail Information
Publications
Restoring function after spinal cord injury: promoting spontaneous regeneration with stem cells and activity-based therapiesVisar 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....
Electrical stimulation promotes the survival of oligodendrocytes in mixed cortical culturesDevin 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...- Investigation of RNA interference to suppress expression of full-length and fragment human huntingtinDevin 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.... 
Functional electrical stimulation helps replenish progenitor cells in the injured spinal cord of adult ratsDaniel 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...- Suppression of calcium release from inositol 1,4,5-trisphosphate-sensitive stores mediates the anti-apoptotic function of nuclear factor-kappaBSimonetta 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... - Essential role for integrin linked kinase in Akt-mediated integrin survival signaling in hippocampal neuronsDevin 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... - PTEN regulates Akt kinase activity in hippocampal neurons and increases their sensitivity to glutamate and apoptosisDevin 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... - Neural stem cells reduce brain injury after unilateral carotid ligationAnne 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... - Involvement of Gadd153 in the pathogenic action of presenilin-1 mutationsOllivier 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... - Neuroprotective and neurorestorative signal transduction mechanisms in brain aging: modification by genes, diet and behaviorMark 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... - RNA interference in biology and medicineOllivier 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... - Matrix metalloproteinase-1 activates a pertussis toxin-sensitive signaling pathway that stimulates the release of matrix metalloproteinase-9Katherine 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... - Olfactory bulbectomy protects hippocampal pyramidal neurons against excitotoxic deathDevin 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...