Genomes and Genes
Kurt J De Vos
Affiliation: King's College London
- VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasisKurt 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...
- A comparison of in vitro properties of resting SOD1 transgenic microglia reveals evidence of reduced neuroprotective functionSiranush A Sargsyan
Department of Medicine, University of Colorado Denver School of Medicine, CO, USA
BMC Neurosci 12:91. 2011....
- Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondriaGábor 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...
- Neurofilament subunit (NFL) head domain phosphorylation regulates axonal transport of neurofilamentsDarran 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...
- Riluzole protects against glutamate-induced slowing of neurofilament axonal transportAlison 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...
- Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria contentKurt 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...
- Phosphorylation of kinesin light chain 1 at serine 460 modulates binding and trafficking of calsyntenin-1Alessio 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...
- Role of axonal transport in neurodegenerative diseasesKurt 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...
- Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6Caroline 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...
- ER-mitochondria associations are regulated by the VAPB-PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43Radu 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. ..
- Deficiency of the copper chaperone for superoxide dismutase increases amyloid-β productionEmma 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...
- Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neuronsTeresa 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. ..