Kurt J De Vos

Summary

Affiliation: King's College London
Country: UK

Publications

  1. pmc VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis
    Kurt J De Vos
    Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, London SE5 8AF, UK
    Hum Mol Genet 21:1299-311. 2012
  2. pmc A comparison of in vitro properties of resting SOD1 transgenic microglia reveals evidence of reduced neuroprotective function
    Siranush A Sargsyan
    Department of Medicine, University of Colorado Denver School of Medicine, CO, USA
    BMC Neurosci 12:91. 2011
  3. pmc Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondria
    Gábor M Mórotz
    Department of Neuroscience, Institute of Psychiatry, Kings College London, London, UK
    Hum Mol Genet 21:1979-88. 2012
  4. doi Neurofilament subunit (NFL) head domain phosphorylation regulates axonal transport of neurofilaments
    Darran M Yates
    MRC Centre for Neurodegeneration Research, Department of Neuroscience P037, Institute of Psychiatry, King s College London, De Crespigny Park, Denmark Hill, London SE58AF, UK
    Eur J Cell Biol 88:193-202. 2009
  5. pmc ALS/FTD-associated FUS activates GSK-3β to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations
    Radu Stoica
    Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, UK
    EMBO Rep 17:1326-42. 2016
  6. doi Riluzole protects against glutamate-induced slowing of neurofilament axonal transport
    Alison Stevenson
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College, London, UK
    Neurosci Lett 454:161-4. 2009
  7. pmc Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content
    Kurt J De Vos
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, Denmark Hill, London SE5 8AF, UK
    Hum Mol Genet 16:2720-8. 2007
  8. doi Role of axonal transport in neurodegenerative diseases
    Kurt J De Vos
    MRC Center for Neurodegeneration Research, Institute of Psychiatry, King s College, London SE5 8AF, United Kingdom
    Annu Rev Neurosci 31:151-73. 2008
  9. pmc Phosphorylation of kinesin light chain 1 at serine 460 modulates binding and trafficking of calsyntenin-1
    Alessio Vagnoni
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, PO Box 37, De Crespigny Park, Denmark Hill, London SE5 8AF, UK
    J Cell Sci 124:1032-42. 2011
  10. pmc Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6
    Caroline Vance
    Department of Clinical Neuroscience, King s College London, Medical Research Council MRC Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK
    Science 323:1208-11. 2009

Collaborators

Detail Information

Publications14

  1. pmc VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis
    Kurt J De Vos
    Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, London SE5 8AF, UK
    Hum Mol Genet 21:1299-311. 2012
    ..Damage to ER, mitochondria and Ca(2+) homeostasis are all seen in ALS and we discuss the implications of our findings in this context...
  2. pmc A comparison of in vitro properties of resting SOD1 transgenic microglia reveals evidence of reduced neuroprotective function
    Siranush A Sargsyan
    Department of Medicine, University of Colorado Denver School of Medicine, CO, USA
    BMC Neurosci 12:91. 2011
    ....
  3. pmc Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondria
    Gábor M Mórotz
    Department of Neuroscience, Institute of Psychiatry, Kings College London, London, UK
    Hum Mol Genet 21:1979-88. 2012
    ..Our results suggest that ALS mutant VAPBP56S perturbs anterograde mitochondrial axonal transport by disrupting Ca(2+) homeostasis and effecting the Miro1/kinesin-1 interaction with tubulin...
  4. doi Neurofilament subunit (NFL) head domain phosphorylation regulates axonal transport of neurofilaments
    Darran M Yates
    MRC Centre for Neurodegeneration Research, Department of Neuroscience P037, Institute of Psychiatry, King s College London, De Crespigny Park, Denmark Hill, London SE58AF, UK
    Eur J Cell Biol 88:193-202. 2009
    ..Our results suggest that NFL head domain phosphorylation is a regulator of neurofilament axonal transport...
  5. pmc ALS/FTD-associated FUS activates GSK-3β to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations
    Radu Stoica
    Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, Kings College London, London, UK
    EMBO Rep 17:1326-42. 2016
    ..Finally, we demonstrate that the FUS-induced reductions to ER-mitochondria associations and are linked to activation of glycogen synthase kinase-3β (GSK-3β), a kinase already strongly associated with ALS/FTD. ..
  6. doi Riluzole protects against glutamate-induced slowing of neurofilament axonal transport
    Alison Stevenson
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College, London, UK
    Neurosci Lett 454:161-4. 2009
    ..Thus, the anti-glutamatergic properties of riluzole include protection against glutamate-induced changes to neurofilament phosphorylation and transport...
  7. pmc Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content
    Kurt J De Vos
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, Denmark Hill, London SE5 8AF, UK
    Hum Mol Genet 16:2720-8. 2007
    ..Together, such changes to mitochondrial function and distribution are likely to compromise axonal function. These alterations represent some of the earliest pathological features so far reported in neurons of mutant SOD1 transgenic mice...
  8. doi Role of axonal transport in neurodegenerative diseases
    Kurt J De Vos
    MRC Center for Neurodegeneration Research, Institute of Psychiatry, King s College, London SE5 8AF, United Kingdom
    Annu Rev Neurosci 31:151-73. 2008
    ..Indeed, we now know that disruption of axonal transport is an early and perhaps causative event in many of these diseases. Here, we review the role of axonal transport in neurodegenerative disease...
  9. pmc Phosphorylation of kinesin light chain 1 at serine 460 modulates binding and trafficking of calsyntenin-1
    Alessio Vagnoni
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, PO Box 37, De Crespigny Park, Denmark Hill, London SE5 8AF, UK
    J Cell Sci 124:1032-42. 2011
    ..Thus, phosphorylation of KLC1ser460 represents a mechanism for selectively regulating the binding and trafficking of calsyntenin-1...
  10. pmc Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6
    Caroline Vance
    Department of Clinical Neuroscience, King s College London, Medical Research Council MRC Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK
    Science 323:1208-11. 2009
    ..FUS is involved in the regulation of transcription and RNA splicing and transport, and it has functional homology to another ALS gene, TARDBP, which suggests that a common mechanism may underlie motor neuron degeneration...
  11. pmc ER-mitochondria associations are regulated by the VAPB-PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43
    Radu Stoica
    1 Department of Neuroscience, Institute of Psychiatry, Kings College London, London SE5 8AF, UK 2 Clinical Neurosciences, Institute of Psychiatry, Kings College London, London SE5 8AF, UK 3
    Nat Commun 5:3996. 2014
    ..Finally, we show that overexpression of TDP-43 leads to activation of glycogen synthase kinase-3β (GSK-3β) and that GSK-3β regulates the VAPB-PTPIP51 interaction. Our results describe a new pathogenic mechanism for TDP-43. ..
  12. pmc Deficiency of the copper chaperone for superoxide dismutase increases amyloid-β production
    Emma H Gray
    MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King s College London, UK
    J Alzheimers Dis 21:1101-5. 2010
    ..Here we show that loss of CCS increases Aβ production in both CCS knockout neurons and CCS siRNA-treated SHSY5Y cells and that this involves increased AβPP processing at the BACE1 site...
  13. ncbi C9orf72 plays a central role in Rab GTPase-dependent regulation of autophagy
    Christopher P Webster
    a Sheffield Institute for Translational Neuroscience SITraN, Department of Neuroscience, University of Sheffield, Sheffield, UK
    Small Gtpases . 2016
    ..In this Commentary we summarise recent findings supporting the key role of C9orf72 in Rab GTPase-dependent regulation of autophagy and discuss autophagy dysregulation as a pathogenic mechanism in ALS/FTD...
  14. pmc Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neurons
    Teresa Rodriguez-Martin
    King s College London, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Department of Basic and Clinical Neuroscience, London, SE5 9NU, UK Electronic address
    Neurobiol Dis 85:1-10. 2016
    ..These results support the association of mutant tau with detrimental effects on mitochondria and will be of significance for the pathogenesis of tauopathies. ..