Bruce A Citron

Summary

Country: USA

Publications

  1. doi request reprint Transcription factor Sp1 dysregulation in Alzheimer's disease
    Bruce A Citron
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, Florida 33744 4125, USA
    J Neurosci Res 86:2499-504. 2008
  2. doi request reprint Modulation of transcription factor Nrf2 in an in vitro model of traumatic brain injury
    Haris Hatic
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, Florida 33744 4125, USA
    J Neurotrauma 29:1188-96. 2012
  3. doi request reprint Modeling the pathobiology of repetitive traumatic brain injury in immortalized neuronal cell lines
    Michael J Kane
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1425:123-31. 2011
  4. doi request reprint Calcitonin receptor-like receptor expression in rat skeletal muscle fibers
    Hugo L Fernandez
    Neuroscience Research Laboratory, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1371:1-6. 2011
  5. doi request reprint Raf inhibition protects cortical cells against beta-amyloid toxicity
    Valentina Echeverria
    Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Neurosci Lett 444:92-6. 2008
  6. ncbi request reprint Transcription factor p53 in degenerating spinal cords
    David J Eve
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1150:174-81. 2007
  7. ncbi request reprint Tissue transglutaminase during mouse central nervous system development: lack of alternative RNA processing and implications for its role(s) in murine models of neurotrauma and neurodegeneration
    Bruce A Citron
    Molecular Biology, Veterans Affairs Medical Center, 4801 Linwood Boulevard, Kansas City, MO 64128, USA
    Brain Res Mol Brain Res 135:122-33. 2005
  8. ncbi request reprint Abnormality of G-protein-coupled receptor kinases at prodromal and early stages of Alzheimer's disease: an association with early beta-amyloid accumulation
    Zhiming Suo
    Laboratory for Alzheimer s Disease and Aging Research, Veterans Affairs Medical Center, Kansas City, Missouri 64128, USA
    J Neurosci 24:3444-52. 2004
  9. ncbi request reprint Injury-induced "switch" from GTP-regulated to novel GTP-independent isoform of tissue transglutaminase in the rat spinal cord
    Barry W Festoff
    Neurobiology Research Laboratory, Department of Veterans Affairs Medical Center, University of Kansas, 4801 Linwood Blvd, Kansas City, MO 64128, USA
    J Neurochem 81:708-18. 2002
  10. ncbi request reprint Participation of protease-activated receptor-1 in thrombin-induced microglial activation
    Zhiming Suo
    Neurobiology Research Laboratory, Veterans Affairs Medical Center, Kansas City, Missouri 64128, USA
    J Neurochem 80:655-66. 2002

Collaborators

Detail Information

Publications11

  1. doi request reprint Transcription factor Sp1 dysregulation in Alzheimer's disease
    Bruce A Citron
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, Florida 33744 4125, USA
    J Neurosci Res 86:2499-504. 2008
    ..These results indicate that elements of regulatory pathways involving transcription factor Sp1 may be useful targets for therapeutic intervention to prevent or reverse AD...
  2. doi request reprint Modulation of transcription factor Nrf2 in an in vitro model of traumatic brain injury
    Haris Hatic
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, Florida 33744 4125, USA
    J Neurotrauma 29:1188-96. 2012
    ..Neuronal health after insult was improved approximately 50% by tBHQ, indicating that neurons exposed to TBI in vitro can be protected...
  3. doi request reprint Modeling the pathobiology of repetitive traumatic brain injury in immortalized neuronal cell lines
    Michael J Kane
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1425:123-31. 2011
    ..These results indicate that the moderate, repetitive injury reduces viability, numbers and lengths of neurites, and that the neuronal loss mechanism includes caspase activation...
  4. doi request reprint Calcitonin receptor-like receptor expression in rat skeletal muscle fibers
    Hugo L Fernandez
    Neuroscience Research Laboratory, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1371:1-6. 2011
    ..This indicates that previously identified pharmacologic heterogeneity is most likely due to post-translational modifications and interactions...
  5. doi request reprint Raf inhibition protects cortical cells against beta-amyloid toxicity
    Valentina Echeverria
    Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Neurosci Lett 444:92-6. 2008
    ..Our results suggest that Raf inhibition with GW5074 is neuroprotective against Abeta toxicity through a mechanism that involves NFkappaB inhibition...
  6. ncbi request reprint Transcription factor p53 in degenerating spinal cords
    David J Eve
    Laboratory of Molecular Biology, Research and Development 151, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA
    Brain Res 1150:174-81. 2007
    ..These results indicate that p53 plays a functional role in oxidative stress-induced cell death and supports the possibility that elevated p53 could be involved in motor neuron death in ALS and the wobbler mouse...
  7. ncbi request reprint Tissue transglutaminase during mouse central nervous system development: lack of alternative RNA processing and implications for its role(s) in murine models of neurotrauma and neurodegeneration
    Bruce A Citron
    Molecular Biology, Veterans Affairs Medical Center, 4801 Linwood Boulevard, Kansas City, MO 64128, USA
    Brain Res Mol Brain Res 135:122-33. 2005
    ..They further impact on drug discovery paradigms, where modulation of activity may have therapeutic value...
  8. ncbi request reprint Abnormality of G-protein-coupled receptor kinases at prodromal and early stages of Alzheimer's disease: an association with early beta-amyloid accumulation
    Zhiming Suo
    Laboratory for Alzheimer s Disease and Aging Research, Veterans Affairs Medical Center, Kansas City, Missouri 64128, USA
    J Neurosci 24:3444-52. 2004
    ..Together, this study not only discovered a novel link between subthreshold Abeta and GRK dysfunction, it also demonstrated that the GRK abnormality in vivo occurs at prodromal and early stages of AD...
  9. ncbi request reprint Injury-induced "switch" from GTP-regulated to novel GTP-independent isoform of tissue transglutaminase in the rat spinal cord
    Barry W Festoff
    Neurobiology Research Laboratory, Department of Veterans Affairs Medical Center, University of Kansas, 4801 Linwood Blvd, Kansas City, MO 64128, USA
    J Neurochem 81:708-18. 2002
    ..Up-regulation of tTG message and activity following neural injury. with appearance of a truncated GTP-unregulated S form, may represent new approaches to drug targets in neurotrauma...
  10. ncbi request reprint Participation of protease-activated receptor-1 in thrombin-induced microglial activation
    Zhiming Suo
    Neurobiology Research Laboratory, Veterans Affairs Medical Center, Kansas City, Missouri 64128, USA
    J Neurochem 80:655-66. 2002
    ..In addition, strategies aimed at blocking thrombin signaling through PAR1 may be therapeutically valuable for diseases associated with cerebral vascular damage and significant inflammation with microglial activation...
  11. ncbi request reprint Protein crosslinking, tissue transglutaminase, alternative splicing and neurodegeneration
    Bruce A Citron
    Neurobiology Research Laboratory, Veterans Affairs Medical Center, 4801 Linwood Boulevard, Kansas City, MO 64128, USA
    Neurochem Int 40:69-78. 2002
    ....