Yoshitaka Nagai

Summary

Affiliation: Osaka University
Country: Japan

Publications

  1. ncbi request reprint Prevention of polyglutamine oligomerization and neurodegeneration by the peptide inhibitor QBP1 in Drosophila
    Yoshitaka Nagai
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Hum Mol Genet 12:1253-9. 2003
  2. ncbi request reprint A toxic monomeric conformer of the polyglutamine protein
    Yoshitaka Nagai
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Nat Struct Mol Biol 14:332-40. 2007
  3. ncbi request reprint [Toxic conformer of the polyglutamine protein]
    Yoshitaka Nagai
    Tanpakushitsu Kakusan Koso 53:235-41. 2008
  4. pmc Residual laminin-binding activity and enhanced dystroglycan glycosylation by LARGE in novel model mice to dystroglycanopathy
    Motoi Kanagawa
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    Hum Mol Genet 18:621-31. 2009
  5. pmc Heat shock transcription factor 1-activating compounds suppress polyglutamine-induced neurodegeneration through induction of multiple molecular chaperones
    Nobuhiro Fujikake
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    J Biol Chem 283:26188-97. 2008
  6. ncbi request reprint Protein transduction domain-mediated delivery of QBP1 suppresses polyglutamine-induced neurodegeneration in vivo
    H Akiko Popiel
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    Mol Ther 15:303-9. 2007
  7. ncbi request reprint Molecular interaction between fukutin and POMGnT1 in the glycosylation pathway of alpha-dystroglycan
    Hui Xiong
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Biochem Biophys Res Commun 350:935-41. 2006
  8. ncbi request reprint Disruption of the toxic conformation of the expanded polyglutamine stretch leads to suppression of aggregate formation and cytotoxicity
    Helena A Popiel
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka, Japan
    Biochem Biophys Res Commun 317:1200-6. 2004
  9. doi request reprint Delivery of the aggregate inhibitor peptide QBP1 into the mouse brain using PTDs and its therapeutic effect on polyglutamine disease mice
    H Akiko Popiel
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Neurosci Lett 449:87-92. 2009
  10. ncbi request reprint Effects of fukutin deficiency in the developing mouse brain
    Tomohiro Chiyonobu
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Neuromuscul Disord 15:416-26. 2005

Collaborators

Detail Information

Publications22

  1. ncbi request reprint Prevention of polyglutamine oligomerization and neurodegeneration by the peptide inhibitor QBP1 in Drosophila
    Yoshitaka Nagai
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Hum Mol Genet 12:1253-9. 2003
    ..The peptide inhibitor QBP1 is a promising candidate with great potential as a therapeutic molecule against the currently untreatable polyQ diseases...
  2. ncbi request reprint A toxic monomeric conformer of the polyglutamine protein
    Yoshitaka Nagai
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Nat Struct Mol Biol 14:332-40. 2007
    ..We conclude that the toxic conformational transition, and not simply the aggregation process itself, is a therapeutic target for polyQ diseases and possibly for conformational diseases in general...
  3. ncbi request reprint [Toxic conformer of the polyglutamine protein]
    Yoshitaka Nagai
    Tanpakushitsu Kakusan Koso 53:235-41. 2008
  4. pmc Residual laminin-binding activity and enhanced dystroglycan glycosylation by LARGE in novel model mice to dystroglycanopathy
    Motoi Kanagawa
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    Hum Mol Genet 18:621-31. 2009
    ....
  5. pmc Heat shock transcription factor 1-activating compounds suppress polyglutamine-induced neurodegeneration through induction of multiple molecular chaperones
    Nobuhiro Fujikake
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    J Biol Chem 283:26188-97. 2008
    ..Our study indicates that induction of multiple molecular chaperones by 17-AAG treatment is a promising therapeutic approach for a wide range of polyQ diseases and possibly other neurodegenerative diseases...
  6. ncbi request reprint Protein transduction domain-mediated delivery of QBP1 suppresses polyglutamine-induced neurodegeneration in vivo
    H Akiko Popiel
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
    Mol Ther 15:303-9. 2007
    ..Our study indicates that PTD-mediated delivery of aggregate inhibitor peptides is a promising therapeutic strategy for neurodegenerative diseases with abnormal aggregation of misfolded proteins...
  7. ncbi request reprint Molecular interaction between fukutin and POMGnT1 in the glycosylation pathway of alpha-dystroglycan
    Hui Xiong
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Biochem Biophys Res Commun 350:935-41. 2006
    ..From these findings, we propose that fukutin forms a complex with POMGnT1 and may modulate its enzymatic activity...
  8. ncbi request reprint Disruption of the toxic conformation of the expanded polyglutamine stretch leads to suppression of aggregate formation and cytotoxicity
    Helena A Popiel
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka, Japan
    Biochem Biophys Res Commun 317:1200-6. 2004
    ..These results show that a gain in toxic conformation of the expanded polyQ protein is essential for aggregation and cytotoxicity, providing insight into establishing therapies against the polyQ diseases...
  9. doi request reprint Delivery of the aggregate inhibitor peptide QBP1 into the mouse brain using PTDs and its therapeutic effect on polyglutamine disease mice
    H Akiko Popiel
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Neurosci Lett 449:87-92. 2009
    ..Our study indicates the potential of PTD-mediated delivery of QBP1 as a therapeutic strategy for the currently untreatable polyQ diseases...
  10. ncbi request reprint Effects of fukutin deficiency in the developing mouse brain
    Tomohiro Chiyonobu
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    Neuromuscul Disord 15:416-26. 2005
    ....
  11. ncbi request reprint [Therapeutic strategies for the polyglutamine diseases]
    Yoshitaka Nagai
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, 2 2 Yamada oka, Suita, Osaka, Japan
    Brain Nerve 59:393-404. 2007
    ..Standardized validation of these preclinical studies and development of sensitive biomarkers for evaluation of therapeutic efficacy in clinical trials will be necessary for development of drugs for the polyglutamine diseases...
  12. ncbi request reprint Conformational changes and aggregation of expanded polyglutamine proteins as therapeutic targets of the polyglutamine diseases: exposed beta-sheet hypothesis
    Yoshitaka Nagai
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Curr Pharm Des 14:3267-79. 2008
    ..We hope that protein aggregate inhibitors which are widely effective not only for the polyQ diseases, but also for many neurodegenerative diseases will be discovered in the near future...
  13. ncbi request reprint Alternative splicing regulates the transcriptional activity of Drosophila heat shock transcription factor in response to heat/cold stress
    Nobuhiro Fujikake
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    FEBS Lett 579:3842-8. 2005
    ..The dHSFc and dHSFd isoforms showed greater transcriptional activity than the other isoforms. Our findings suggest that alternative splicing regulates the transcriptional activity of dHSF...
  14. ncbi request reprint Multiple candidate gene analysis identifies alpha-synuclein as a susceptibility gene for sporadic Parkinson's disease
    Ikuko Mizuta
    Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, Osaka, Japan
    Hum Mol Genet 15:1151-8. 2006
    ..SNCA expression levels tended to be positively correlated with the number of the associated allele in autopsied frontal cortices. These findings establish SNCA as a definite susceptibility gene for sporadic PD...
  15. ncbi request reprint Fukuyama-type congenital muscular dystrophy (FCMD) and alpha-dystroglycanopathy
    Tatsushi Toda
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, Suita, Osaka 565 0871, Japan
    Congenit Anom (Kyoto) 43:97-104. 2003
    ..In this review Fukuyama-type congenital muscular dystrophy (FCMD), other CMDs with brain malformations, and their relation with alpha-dystroglycan are discussed...
  16. ncbi request reprint Identification of CAG repeat-containing genes expressed in human brain as candidate genes for autosomal dominant spinocerebellar ataxias and other neurodegenerative diseases
    Masaji Tachikawa
    Division of Functional Genomics, Department of Post Genomics and Diseases, Osaka University Graduate School of Medicine, 2 2 B9 Yamadaoka, Suita, Osaka 565 0871, Japan
    J Hum Genet 47:275-8. 2002
    ....
  17. ncbi request reprint Soluble polyglutamine oligomers formed prior to inclusion body formation are cytotoxic
    Toshiaki Takahashi
    School of Health Sciences, Faculty of Medicine, Niigata University, 1 757 Asahimachi, Niigata 951 8122, Japan
    Hum Mol Genet 17:345-56. 2008
    ..These results indicate that a length-dependent formation of oligomers is an essential mechanism underlying neurodegeneration in polyQ-mediated disorders...
  18. ncbi request reprint Detection of polyglutamine protein oligomers in cells by fluorescence correlation spectroscopy
    Yasuo Takahashi
    Laboratory of Supramolecular Biophysics, Research Institute for Electronic Science, Hokkaido University, Sapporo, Hokkaido 060 0812, Japan
    J Biol Chem 282:24039-48. 2007
    ..We therefore conclude that FCS is a useful technique to monitor the oligomerization of disease-causing proteins in cells as well as its inhibition in the conformational diseases...
  19. ncbi request reprint Cytoprotective effect of novel histone deacetylase inhibitors against polyglutamine toxicity
    Shingo Kariya
    Department of Neurology, Nara Medical University, Kashihara, Japan
    Neurosci Lett 392:213-5. 2006
    ..Although our study showed mild neuroprotective effects, further structural modification of compounds that retain this residue may decrease cytotoxicity and increase protective activity against polyQ toxicity...
  20. doi request reprint Suppression of mutant Huntingtin aggregate formation by Cdk5/p35 through the effect on microtubule stability
    Sayuko Kaminosono
    Department of Biological Sciences, Tokyo Metropolitan University, Hachioji, Tokyo 192 0397, Japan
    J Neurosci 28:8747-55. 2008
    ..This Cdk5 inhibition of htt aggregates is a novel mechanism different from htt phosphorylation and interaction with Cdk5 reported previously (Luo et al., 2005; Anne et al., 2007)...
  21. ncbi request reprint Glycosylation of the alpha and beta tubulin by sialyloligosaccharides
    Mizuki Hino
    Department of Biological Science, Graduate School of Science, Hiroshima University, Hiroshima, Japan
    Zoolog Sci 20:709-15. 2003
    ..These results indicate that alpha and beta tubulin are glycosylated with sialyloligosaccharides...
  22. ncbi request reprint Humanin attenuates apoptosis induced by DRPLA proteins with expanded polyglutamine stretches
    Shingo Kariya
    Department of Neurology, Nara Medical University, Nara, 634 8522, Japan
    J Mol Neurosci 25:165-9. 2005
    ..Although the details remain uncertain, our results suggest that ASK1 is potentially involved in pathogenesis of DRPLA and that HN might contribute partially to the suppression of neurodegeneration in polyQ diseases...