F Usuki

Summary

Affiliation: National Institute for Minamata Disease
Country: Japan

Publications

  1. pmc Endoplasmic reticulum stress preconditioning attenuates methylmercury-induced cellular damage by inducing favorable stress responses
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Sci Rep 3:2346. 2013
  2. ncbi request reprint Differential signaling pathways following oxidative stress in mutant myotonin protein kinase cDNA-transfected C2C12 cell lines
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata, 867 0008, Japan
    Biochem Biophys Res Commun 267:739-43. 2000
  3. pmc Ataxia caused by mutations in the alpha-tocopherol transfer protein gene
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    J Neurol Neurosurg Psychiatry 69:254-6. 2000
  4. ncbi request reprint In vivo protection of a water-soluble derivative of vitamin E, Trolox, against methylmercury-intoxication in the rat
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Neurosci Lett 304:199-203. 2001
  5. ncbi request reprint Beneficial effects of mild lifelong dietary restriction on skeletal muscle: prevention of age-related mitochondrial damage, morphological changes, and vulnerability to a chemical toxin
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, 867 0008, Minamata, Japan
    Acta Neuropathol 108:1-9. 2004
  6. pmc Post-transcriptional defects of antioxidant selenoenzymes cause oxidative stress under methylmercury exposure
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    J Biol Chem 286:6641-9. 2011
  7. ncbi request reprint Specific inhibition of nonsense-mediated mRNA decay components, SMG-1 or Upf1, rescues the phenotype of Ullrich disease fibroblasts
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Mol Ther 14:351-60. 2006
  8. ncbi request reprint Methylmercury activates ASK1/JNK signaling pathways, leading to apoptosis due to both mitochondria- and endoplasmic reticulum (ER)-generated processes in myogenic cell lines
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata, Kumamoto 867 0008, Japan
    Neurotoxicology 29:22-30. 2008
  9. ncbi request reprint The effect of methylmercury on skeletal muscle in the rat: a histopathological study
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, Hama, Japan
    Toxicol Lett 94:227-32. 1998
  10. doi request reprint Methylmercury exposure downregulates the expression of Racl and leads to neuritic degeneration and ultimately apoptosis in cerebrocortical neurons
    Masatake Fujimura
    Department of Basic Medical Sciences, National Institute for Minamata Disease, Kumamoto, Japan
    Neurotoxicology 30:16-22. 2009

Detail Information

Publications14

  1. pmc Endoplasmic reticulum stress preconditioning attenuates methylmercury-induced cellular damage by inducing favorable stress responses
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Sci Rep 3:2346. 2013
    ....
  2. ncbi request reprint Differential signaling pathways following oxidative stress in mutant myotonin protein kinase cDNA-transfected C2C12 cell lines
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata, 867 0008, Japan
    Biochem Biophys Res Commun 267:739-43. 2000
    ..These results suggest that the susceptibility to oxidative stress in mutant MtPK cDNA transformants involves differential signaling pathways evoked following oxidative stress...
  3. pmc Ataxia caused by mutations in the alpha-tocopherol transfer protein gene
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    J Neurol Neurosurg Psychiatry 69:254-6. 2000
    ..Supplementary therapy increased her serum vitamin E concentration to the normal range with mild improvement of the deep senses...
  4. ncbi request reprint In vivo protection of a water-soluble derivative of vitamin E, Trolox, against methylmercury-intoxication in the rat
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Neurosci Lett 304:199-203. 2001
    ..These data indicate that MeHg-mediated oxidative stress plays an important role in the in vivo pathological process of MeHg intoxication. Trolox may prevent some of clinical manifestations of MeHg-intoxication in humans...
  5. ncbi request reprint Beneficial effects of mild lifelong dietary restriction on skeletal muscle: prevention of age-related mitochondrial damage, morphological changes, and vulnerability to a chemical toxin
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, 867 0008, Minamata, Japan
    Acta Neuropathol 108:1-9. 2004
    ..The results indicate that mild lifelong DR also protects skeletal muscle and peripheral nerves against a chemically-induced form of oxidative stress...
  6. pmc Post-transcriptional defects of antioxidant selenoenzymes cause oxidative stress under methylmercury exposure
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    J Biol Chem 286:6641-9. 2011
    ..Treatment with ebselen, a seleno-organic compound, effectively suppressed oxidative stress and protected cells against MeHg-induced relative selenium deficiency and cytotoxicity...
  7. ncbi request reprint Specific inhibition of nonsense-mediated mRNA decay components, SMG-1 or Upf1, rescues the phenotype of Ullrich disease fibroblasts
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata 867 0008, Japan
    Mol Ther 14:351-60. 2006
    ..We suggest that the inhibition of NMD may be useful as a therapeutic approach to treat some human genetic diseases exacerbated by NMD...
  8. ncbi request reprint Methylmercury activates ASK1/JNK signaling pathways, leading to apoptosis due to both mitochondria- and endoplasmic reticulum (ER)-generated processes in myogenic cell lines
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, 4058 18 Hama, Minamata, Kumamoto 867 0008, Japan
    Neurotoxicology 29:22-30. 2008
    ..Combined treatment with protective factors against oxidative and ER stresses is necessary, especially in the later stages of MeHg cytotoxicity...
  9. ncbi request reprint The effect of methylmercury on skeletal muscle in the rat: a histopathological study
    F Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, Hama, Japan
    Toxicol Lett 94:227-32. 1998
    ..These changes were more prominent in mitochondria-rich soleus muscle than in extensor digitorum longus muscle. Our findings confirm that MeHg exposure disturbs mitochondrial energy metabolism in skeletal muscle...
  10. doi request reprint Methylmercury exposure downregulates the expression of Racl and leads to neuritic degeneration and ultimately apoptosis in cerebrocortical neurons
    Masatake Fujimura
    Department of Basic Medical Sciences, National Institute for Minamata Disease, Kumamoto, Japan
    Neurotoxicology 30:16-22. 2009
    ..The results indicate that neuritic degeneration, in particular axonal degeneration triggered by the downregulation of Rac1 expression, contributes to MeHg-induced apoptotic cell death in cultured cerebrocortical neurons...
  11. doi request reprint Methylmercury induces neuropathological changes with tau hyperphosphorylation mainly through the activation of the c-jun-N-terminal kinase pathway in the cerebral cortex, but not in the hippocampus of the mouse brain
    Masatake Fujimura
    Department of Basic Medical Sciences, National Institute for Minamata Disease, 4058 18 Hama, Minamata, Kumamoto 867 0008, Japan
    Neurotoxicology 30:1000-7. 2009
    ....
  12. doi request reprint Inhibition of the Rho/ROCK pathway prevents neuronal degeneration in vitro and in vivo following methylmercury exposure
    Masatake Fujimura
    Department of Basic Medical Sciences, National Institute for Minamata Disease, Kumamoto, Japan
    Toxicol Appl Pharmacol 250:1-9. 2011
    ..The results suggest that inhibition of the Rho/ROCK pathway rescues MeHg-mediated neuritic extension/retraction incoordination and is effective for the prevention of MeHg-induced axonal degeneration and apoptotic neuronal cell death...
  13. ncbi request reprint Inhibition of nonsense-mediated mRNA decay rescues the phenotype in Ullrich's disease
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease, Hama, Minamata, Japan
    Ann Neurol 55:740-4. 2004
    ..Our results suggest that NMD inhibitors can be used as a therapeutic tool to rescue some human genetic diseases exacerbated by NMD...
  14. ncbi request reprint [Specific inhibition of nonsense-mediated mRNA decay has the potential to rescue the phenotype of muscular dystrophy]
    Fusako Usuki
    Department of Clinical Medicine, National Institute for Minamata Disease
    Rinsho Shinkeigaku 46:939-41. 2006
    ..The results suggest that specific inhibition of NMD may be useful as a therapeutic approach to treat some human genetic diseases exacerbated by NMD...