Kenneth M Rosen

Summary

Affiliation: Tufts University School of Medicine
Country: USA

Publications

  1. ncbi Downregulation and increased turnover of beta-amyloid precursor protein in skeletal muscle cultures by neuregulin-1
    Kenneth M Rosen
    Division of Neurology, St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Exp Neurol 181:170-80. 2003
  2. ncbi Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells
    Kenneth M Rosen
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:12809-16. 2006
  3. pmc Parkin reverses intracellular beta-amyloid accumulation and its negative effects on proteasome function
    Kenneth M Rosen
    Department of Neurology, Tufts University School of Medicine, Boston, Massachusetts, USA
    J Neurosci Res 88:167-78. 2010
  4. ncbi CHIP and HSPs interact with beta-APP in a proteasome-dependent manner and influence Abeta metabolism
    Pravir Kumar
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Hum Mol Genet 16:848-64. 2007
  5. ncbi Transgenic expression of beta-APP in fast-twitch skeletal muscle leads to calcium dyshomeostasis and IBM-like pathology
    Charbel E H Moussa
    Department of Neurology, Caritas St Elizabeth s Medical Center of Boston, Tufts University School of Medicine, 736 Cambridge St, Boston, MA, USA
    FASEB J 20:2165-7. 2006
  6. pmc The insulin/Akt signaling pathway is targeted by intracellular beta-amyloid
    Han Kyu Lee
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Mol Biol Cell 20:1533-44. 2009
  7. ncbi Dissociation of ERK and Akt signaling in endothelial cell angiogenic responses to beta-amyloid
    Jordi Magrane
    Department of Neurology, Caritas St Elizabeth s Medical Center and Tufts University School of Medicine, Boston, MA 02135, USA
    Exp Cell Res 312:996-1010. 2006
  8. ncbi Differential effects of mitochondrial heat shock protein 60 and related molecular chaperones to prevent intracellular beta-amyloid-induced inhibition of complex IV and limit apoptosis
    Vimal Veereshwarayya
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:29468-78. 2006
  9. ncbi Intraneuronal beta-amyloid expression downregulates the Akt survival pathway and blunts the stress response
    Jordi Magrane
    Department of Neurology, Caritas Saint Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Neurosci 25:10960-9. 2005
  10. ncbi Nerve injury induces glial cell line-derived neurotrophic factor (GDNF) expression in Schwann cells through purinergic signaling and the PKC-PKD pathway
    Pin Xu
    F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, MA, USA
    Glia 61:1029-40. 2013

Collaborators

Detail Information

Publications12

  1. ncbi Downregulation and increased turnover of beta-amyloid precursor protein in skeletal muscle cultures by neuregulin-1
    Kenneth M Rosen
    Division of Neurology, St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Exp Neurol 181:170-80. 2003
    ..BetaAPP should be added to the list of specialized post-neuromuscular junction proteins that are regulated by cholinergic terminal-derived factors critical to synaptogenesis...
  2. ncbi Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells
    Kenneth M Rosen
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:12809-16. 2006
    ..These data support the hypothesis that in myocytes parkin has dual properties in the maintenance of skeletal muscle mitochondrial homeostasis and in the regulation of A beta levels...
  3. pmc Parkin reverses intracellular beta-amyloid accumulation and its negative effects on proteasome function
    Kenneth M Rosen
    Department of Neurology, Tufts University School of Medicine, Boston, Massachusetts, USA
    J Neurosci Res 88:167-78. 2010
    ..In AD brain, Parkin was found to interact with Abeta and its levels were reduced. Thus, Parkin is cytoprotective, partially by increasing the removal of cellular Abeta through a proteasome-dependent pathway...
  4. ncbi CHIP and HSPs interact with beta-APP in a proteasome-dependent manner and influence Abeta metabolism
    Pravir Kumar
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Hum Mol Genet 16:848-64. 2007
    ..CHIP also hastens the clearance of Abeta in a manner consistent with its known neuroprotective properties...
  5. ncbi Transgenic expression of beta-APP in fast-twitch skeletal muscle leads to calcium dyshomeostasis and IBM-like pathology
    Charbel E H Moussa
    Department of Neurology, Caritas St Elizabeth s Medical Center of Boston, Tufts University School of Medicine, 736 Cambridge St, Boston, MA, USA
    FASEB J 20:2165-7. 2006
    ..The increase in resting calcium and depolarization are novel findings, suggesting both a mechanism for the weakness and an avenue for therapeutic intervention in IBM...
  6. pmc The insulin/Akt signaling pathway is targeted by intracellular beta-amyloid
    Han Kyu Lee
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Mol Biol Cell 20:1533-44. 2009
    ..Importantly, Abeta did not interrupt Akt or PI3K activities (once stimulated) nor did it affect more proximal signal events. These results offer a novel therapeutic strategy to neutralize Abeta-induced energy failure and neuronal death...
  7. ncbi Dissociation of ERK and Akt signaling in endothelial cell angiogenic responses to beta-amyloid
    Jordi Magrane
    Department of Neurology, Caritas St Elizabeth s Medical Center and Tufts University School of Medicine, Boston, MA 02135, USA
    Exp Cell Res 312:996-1010. 2006
    ..The marked effect of extracellular Abeta on the migration component of angiogenesis is associated with inhibition of MAPK signaling, while Akt-dependent cell survival appears more affected by cellular Abeta...
  8. ncbi Differential effects of mitochondrial heat shock protein 60 and related molecular chaperones to prevent intracellular beta-amyloid-induced inhibition of complex IV and limit apoptosis
    Vimal Veereshwarayya
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:29468-78. 2006
    ..The combined effect of HSPs was to reduce the free radical burden, preserve ATP generation, decrease cytochrome c release, and prevent caspase-9 activation, all important mediators of beta-amyloid-induced neuronal dysfunction and death...
  9. ncbi Intraneuronal beta-amyloid expression downregulates the Akt survival pathway and blunts the stress response
    Jordi Magrane
    Department of Neurology, Caritas Saint Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Neurosci 25:10960-9. 2005
    ..These results suggest that the early dysfunction associated with intraneuronal Abeta accumulation in AD involve the associated impairments of Akt signaling and suppression of the stress response...
  10. ncbi Nerve injury induces glial cell line-derived neurotrophic factor (GDNF) expression in Schwann cells through purinergic signaling and the PKC-PKD pathway
    Pin Xu
    F M Kirby Neurobiology Center, Children s Hospital Boston, Boston, MA, USA
    Glia 61:1029-40. 2013
    ..Given the potent effects of GDNF on survival and repair of injured peripheral neurons, we propose that targeting these pathways may yield therapeutic tools to treat peripheral nerve injury and neuropathies...
  11. pmc Activity dependent localization of synaptic NMDA receptors in spinal neurons
    Kenneth M Rosen
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Mol Cell Neurosci 34:578-91. 2007
    ....
  12. pmc Cell-free embryonic stem cell extract-mediated derivation of multipotent stem cells from NIH3T3 fibroblasts for functional and anatomical ischemic tissue repair
    Johnson Rajasingh
    Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, 303 E Chicago Ave, Chicago IL 60611, USA
    Circ Res 102:e107-17. 2008
    ..These data provide evidence for the generation of functional multipotent stem-like cells from terminally differentiated somatic cells without the introduction of retroviral mediated transgenes or ESC fusion...