Vos, Kurt De - University of Sheffield - Department of Neuroscience

个人简介

2011-present Lecturer in Translational Neuroscience 2006-2011 Senior Researcher, MRC Centre for Neurodegeneration Research, The Institute of Psychiatry, King's College London, London, UK. 2004-2006 Postdoctoral Researcher, Academic Unit of Neurology, The University of Sheffield, Sheffield, UK. 2003-2004 Postdoctoral Researcher/Visiting Scientist, School of Biological Sciences, University of Manchester, Manchester, UK. 2000-2003 Postdoctoral Researcher, Department of Biological Sciences, Columbia University, New York, USA. 1994-1999 PhD in Science: Biotechnology (Greatest distinction), University of Ghent, Ghent, Belgium. Dr De Vos studied chemistry and biotechnology and received a PhD in Biotechnology with greatest distinction from Ghent University, Belgium (1999; advisor Prof Johan Grooten). There he showed that clustering of mitochondria in the perinuclear region is an early event in apoptosis that is caused by inhibition of the molecular motor kinesin through hyperphosphorylation of the kinesin light chain (De Vos et al., 1998; De Vos et al., 2000). He then embarked on his postdoctoral research work in the laboratories of Prof Mike Sheetz at Columbia University, New York, and Dr Vicky Allan at the University of Manchester. There he showed that phosphatidyl inositol phosphates control the direction of axonal mitochondrial transport (De Vos et al., 2003). In addition he established that mitochondrial function controls mitochondrial dynamics and showed that the actin cytoskeleton is required for the recruitment of mitochondrial fission factor DRP1 to mitochondria (De Vos et al., 2005). He became particularly interested in mitochondrial dynamics and neurodegeneration and relocated to the University of Sheffield to work in Dr Andy Grierson’s laboratory. There his research was focused on motor neuron diseases and the characterisation of mitochondrial axonal transport defects in models of amyotrophic lateral sclerosis (ALS) and hereditary spastic paraplegia (De Vos et al., 2007; Kasher et al., 2009). This work was continued in the laboratory of Prof Chris Miller and Prof Chris Shaw in the MRC Centre for Neurodegeneration Research at King’s College London, and resulted in publications showing that VAPB interacts with mitochondrial protein PTPIP51 and that ALS VAPBP56S the disrupts axonal transport of mitochondria by increasing intracellular calcium levels. End of 2011 he returned to Sheffield and took up the post of Lecturer in Translational Neuroscience in the newly established Sheffield Institute for Translational Neuroscience (SITRaN).

研究领域

Research in the laboratory focuses on the mechanisms of nerve cell death in amyotrophic lateral sclerosis (ALS; also known as motor neuron disease (MND) or Lou Gehrig disease), hereditary spastic paraplegia (HSP) and Parkinson’s disease (PD). We are especially interested in the involvement of axonal transport, mitochondria and ER. Current research themes include: The mechanisms causing defective axonal transport of mitochondria in ALS, PD and HSP. The cellular roles of C9ORF72 protein and their role in ALS and FTD The biology of close contacts between the endoplasmic reticulum (ER) and mitochondria and their involvement in health and disease

近期论文

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Chapman, A.L., et al., Axonal Transport Defects in a Mitofusin 2 Loss of Function Model of Charcot-Marie-Tooth Disease in Zebrafish. PLoS One, 2013. 8(6): p. e67276. Morotz, G.M., et al., Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondria. Hum Mol Genet, 2012. 21(9): p. 1979-88. De Vos, K.J., et al., VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis. Hum Mol Genet, 2012. 21(6): p. 1299-311. Vagnoni, A., et al., Phosphorylation of kinesin light chain 1 at serine 460 modulates binding and trafficking of calsyntenin-1. Journal of Cell Science, 2011. 124(Pt 7): p. 1032-1042. Sargsyan, S.A., et al., A comparison of in vitro properties of resting SOD1 transgenic microglia reveals evidence of reduced neuroprotective function. BMC neuroscience, 2011. 12(1): p. 91. Manser, C., et al., Lemur tyrosine kinase-2 signalling regulates kinesin-1 light chain-2 phosphorylation and binding of Smad2 cargo. Oncogene, 2011: p. -.