Bradley J Turner

Summary

Affiliation: University of Melbourne
Country: Australia

Publications

  1. ncbi Behavioural and anatomical effects of systemically administered leukemia inhibitory factor in the SOD1(G93A G1H) mouse model of familial amyotrophic lateral sclerosis
    Michael F Azari
    Department of Anatomy and Cell Biology, Faculty of Medicine, P O Box 13C, Monash University, 3800 Victoria, Australia
    Brain Res 982:92-7. 2003
  2. doi Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS
    Bradley J Turner
    MRC Functional Genetics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK
    Prog Neurobiol 85:94-134. 2008
  3. pmc TDP-43 expression in mouse models of amyotrophic lateral sclerosis and spinal muscular atrophy
    Bradley J Turner
    University of Oxford, MRC Functional Genetics Unit, Department of Physiology, Anatomy and Genetics, South Parks Road, Oxford, OX1 3QX, UK
    BMC Neurosci 9:104. 2008
  4. pmc Overexpression of survival motor neuron improves neuromuscular function and motor neuron survival in mutant SOD1 mice
    Bradley J Turner
    Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia Centre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia Electronic address
    Neurobiol Aging 35:906-15. 2014
  5. doi Survival motor neuron deficiency enhances progression in an amyotrophic lateral sclerosis mouse model
    Bradley J Turner
    MRC Functional Genomics Unit, University of Oxford, Department of Physiology, Anatomy and Genetics, Oxford, UK
    Neurobiol Dis 34:511-7. 2009
  6. ncbi Induction of the unfolded protein response in familial amyotrophic lateral sclerosis and association of protein-disulfide isomerase with superoxide dismutase 1
    Julie D Atkin
    Brain Injury and Repair Group, Howard Florey Institute, University of Melbourne, Parkville, Victoria 3010, USA
    J Biol Chem 281:30152-65. 2006
  7. doi Serum matrix metalloproteinase-9 activity is dysregulated with disease progression in the mutant SOD1 transgenic mice
    Cynthia P W Soon
    Department of Pathology, The University of Melbourne, Parkville, VIC 3010, Australia
    Neuromuscul Disord 20:260-6. 2010
  8. ncbi Mutant SOD1 inhibits ER-Golgi transport in amyotrophic lateral sclerosis
    Julie D Atkin
    Department of Biochemistry, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Melbourne, Australia Department of Florey Neuroscience, University of Melbourne, Parkville, Melbourne, Australia
    J Neurochem 129:190-204. 2014
  9. ncbi Brain beta-amyloid accumulation in transgenic mice expressing mutant superoxide dismutase 1
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria 3010, Australia
    Neurochem Res 29:2281-6. 2004
  10. ncbi Impaired extracellular secretion of mutant superoxide dismutase 1 associates with neurotoxicity in familial amyotrophic lateral sclerosis
    Bradley J Turner
    Motor Neuron Disease Research Laboratory, Brain Injury and Repair Group, Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria 3010, Australia
    J Neurosci 25:108-17. 2005

Collaborators

Detail Information

Publications22

  1. ncbi Behavioural and anatomical effects of systemically administered leukemia inhibitory factor in the SOD1(G93A G1H) mouse model of familial amyotrophic lateral sclerosis
    Michael F Azari
    Department of Anatomy and Cell Biology, Faculty of Medicine, P O Box 13C, Monash University, 3800 Victoria, Australia
    Brain Res 982:92-7. 2003
    ..However, we found no significant rescue of motoneurons or prolongation of survival as a result of this systemic dose of LIF in these mice...
  2. doi Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS
    Bradley J Turner
    MRC Functional Genetics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK
    Prog Neurobiol 85:94-134. 2008
    ..This review summarises the wealth of known genetic and therapeutic modifiers in rodent models with SOD1 mutations and discusses these in the wider context of ALS pathoetiology and treatment...
  3. pmc TDP-43 expression in mouse models of amyotrophic lateral sclerosis and spinal muscular atrophy
    Bradley J Turner
    University of Oxford, MRC Functional Genetics Unit, Department of Physiology, Anatomy and Genetics, South Parks Road, Oxford, OX1 3QX, UK
    BMC Neurosci 9:104. 2008
    ..Here, we characterise TDP-43 localisation, expression levels and post-translational modifications in mouse models of ALS and spinal muscular atrophy (SMA)...
  4. pmc Overexpression of survival motor neuron improves neuromuscular function and motor neuron survival in mutant SOD1 mice
    Bradley J Turner
    Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia Centre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia Electronic address
    Neurobiol Aging 35:906-15. 2014
    ..Studies in emerging mouse models of ALS are therefore warranted to further explore the potential of SMN as a modifier of ALS. ..
  5. doi Survival motor neuron deficiency enhances progression in an amyotrophic lateral sclerosis mouse model
    Bradley J Turner
    MRC Functional Genomics Unit, University of Oxford, Department of Physiology, Anatomy and Genetics, Oxford, UK
    Neurobiol Dis 34:511-7. 2009
    ..We therefore propose that SMN replacement and upregulation strategies considered for SMA therapy may have protective potential for ALS...
  6. ncbi Induction of the unfolded protein response in familial amyotrophic lateral sclerosis and association of protein-disulfide isomerase with superoxide dismutase 1
    Julie D Atkin
    Brain Injury and Repair Group, Howard Florey Institute, University of Melbourne, Parkville, Victoria 3010, USA
    J Biol Chem 281:30152-65. 2006
    ..The possibility that PDI may be a therapeutic target to prevent SOD1 aggregation is also raised by this study...
  7. doi Serum matrix metalloproteinase-9 activity is dysregulated with disease progression in the mutant SOD1 transgenic mice
    Cynthia P W Soon
    Department of Pathology, The University of Melbourne, Parkville, VIC 3010, Australia
    Neuromuscul Disord 20:260-6. 2010
    ..These data indicate that circulating MMP-9 is altered throughout the course of disease progression in mice. Further studies in human ALS may validate the suitability of serum MMP-9 activity as a biomarker for early stage disease...
  8. ncbi Mutant SOD1 inhibits ER-Golgi transport in amyotrophic lateral sclerosis
    Julie D Atkin
    Department of Biochemistry, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Melbourne, Australia Department of Florey Neuroscience, University of Melbourne, Parkville, Melbourne, Australia
    J Neurochem 129:190-204. 2014
    ..These findings thus link several cellular events in amyotrophic lateral sclerosis into a single mechanism occurring early in mSOD1 expressing cells...
  9. ncbi Brain beta-amyloid accumulation in transgenic mice expressing mutant superoxide dismutase 1
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria 3010, Australia
    Neurochem Res 29:2281-6. 2004
    ..We therefore conclude that mutant SOD1 overexpression promotes neither Abeta toxicity nor brain accumulation in these ALS models...
  10. ncbi Impaired extracellular secretion of mutant superoxide dismutase 1 associates with neurotoxicity in familial amyotrophic lateral sclerosis
    Bradley J Turner
    Motor Neuron Disease Research Laboratory, Brain Injury and Repair Group, Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria 3010, Australia
    J Neurosci 25:108-17. 2005
    ..Collectively, these results suggest novel extracellular roles for SOD1 in ALS and support a causal relationship between mutant SOD1 secretion and intraneuronal toxicity...
  11. ncbi Antisense peptide nucleic acid targeting GluR3 delays disease onset and progression in the SOD1 G93A mouse model of familial ALS
    Alan Rembach
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria, Australia
    J Neurosci Res 77:573-82. 2004
    ....
  12. pmc Diacetylbis(N(4)-methylthiosemicarbazonato) copper(II) (CuII(atsm)) protects against peroxynitrite-induced nitrosative damage and prolongs survival in amyotrophic lateral sclerosis mouse model
    Cynthia P W Soon
    Department of Pathology, Mental Health Research Institute, School of Chemistry, The University of Melbourne, Parkville, Victoria, Australia
    J Biol Chem 286:44035-44. 2011
    ..CuII(atsm) therefore represents a potential new class of neuroprotective agents targeting multiple major disease pathways of motor neurons with therapeutic potential for ALS...
  13. ncbi Effect of p75 neurotrophin receptor antagonist on disease progression in transgenic amyotrophic lateral sclerosis mice
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Melbourne, Victoria, Australia
    J Neurosci Res 78:193-9. 2004
    ..Thus, alternate ligand-independent pathways of p75(NTR) activation or additional NGF receptor targets may contribute to motor neuron degeneration in ALS mice...
  14. doi Dismutase-competent SOD1 mutant accumulation in myelinating Schwann cells is not detrimental to normal or transgenic ALS model mice
    Bradley J Turner
    MRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, John Radcliffe Hospital, University of Oxford, Oxford OX1 3QX, UK
    Hum Mol Genet 19:815-24. 2010
    ..We conclude that dismutase-competent mutant SOD1 accumulation within Schwann cells is not pathological to spinal motor neurons or deleterious to disease course in transgenic ALS model mice, in contrast to astrocytes and microglia...
  15. ncbi Inducible superoxide dismutase 1 aggregation in transgenic amyotrophic lateral sclerosis mouse fibroblasts
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria, Australia
    J Cell Biochem 91:1074-84. 2004
    ..We propose that non-neural cultures such as these transgenic fibroblasts with inducible SOD1 aggregation may be useful for rapid screening of compounds with anti-aggregation potential in FALS...
  16. ncbi Neuromuscular accumulation of mutant superoxide dismutase 1 aggregates in a transgenic mouse model of familial amyotrophic lateral sclerosis
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Melbourne, Victoria 3010, Australia
    Neurosci Lett 350:132-6. 2003
    ....
  17. doi HspB8 mutation causing hereditary distal motor neuropathy impairs lysosomal delivery of autophagosomes
    Alice S Kwok
    MRC Functional Genomics Unit, Department of Anatomy Physiology and Genetics, University of Oxford, South Parks Road, Oxford, UK
    J Neurochem 119:1155-61. 2011
    ..We conclude that defects in HspB8-mediated autophagy are likely to contribute to dHMNII pathology and their detection in peripheral blood mononuclear cells could be a useful, accessible biomarker for the disease...
  18. ncbi Antisense peptide nucleic acid-mediated knockdown of the p75 neurotrophin receptor delays motor neuron disease in mutant SOD1 transgenic mice
    Bradley J Turner
    Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia
    J Neurochem 87:752-63. 2003
    ..The uptake of fluorescent-labelled antisense PNA in the nervous system of transgenic mice was also confirmed. This study suggests that p75NTR may be a promising antisense target in the treatment of ALS...
  19. ncbi ER stress and UPR in familial amyotrophic lateral sclerosis
    Bradley J Turner
    Howard Florey Institute, University of Melbourne, Victoria, Australia
    Curr Mol Med 6:79-86. 2006
    ..We propose that ER stress and UPR may be coupled to GA dysfunction in mutant SOD1-mediated toxicity, promoting ER-initiated cell death signalling in FALS...
  20. pmc ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation
    Adam K Walker
    Department of Biochemistry, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Victoria, Australia Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia
    PLoS ONE 8:e81170. 2013
    ..This study provides evidence for ER stress as a pathogenic pathway in TDP-43-mediated disease. ..
  21. pmc Mutant TDP-43 Deregulates AMPK activation by PP2A in ALS models
    Nirma D Perera
    Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Melbourne, Victoria, Australia Centre for Neuroscience, University of Melbourne, Parkville, Melbourne, Victoria, Australia
    PLoS ONE 9:e90449. 2014
    ..While AMPK activation in motor neurons correlateswith progressionin mutant SOD1-mediated disease, AMPK inactivation mediated by PP2Ais associated withmutant TDP-43-linked ALS. ..
  22. ncbi The beta-amyloid peptide of Alzheimer's disease decreases adhesion of vascular smooth muscle cells to the basement membrane
    Su San Mok
    Department of Pathology, University of Melbourne, Parkville, Victoria, Australia
    J Neurochem 96:53-64. 2006
    ..An inhibitor of ERK1/2 phosphorylation enhanced the effect of Abeta on cell adhesion. The studies suggest that Abeta can decrease VSMC viability by disrupting VSMC-extracellular matrix (ECM) adhesion...