Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathway

DOI Web Site 被引用文献4件
  • Hoon Ryu
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Junghee Lee
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Beatrix A. Olofsson
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Aziza Mwidau
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Alpaslan Deodoglu
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Maria Escudero
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Erik Flemington
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Jane Azizkhan-Clifford
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Robert J. Ferrante
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...
  • Rajiv R. Ratan
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115; Department of Biochemistry, Drexel University College of Medicine, Philadelphia, PA 19102; Geriatric Research and Education and Clinical Center, Bedford Veterans Affairs Medical Center, and Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Bedford, MA 01730; and Department of Pathology, Tulane...

書誌事項

公開日
2003-03-14
DOI
  • 10.1073/pnas.0737363100
公開者
Proceedings of the National Academy of Sciences

この論文をさがす

説明

<jats:p> Oxidative stress is believed to be an important mediator of neurodegeneration. However, the transcriptional pathways induced in neurons by oxidative stress that activate protective gene responses have yet to be fully delineated. We report that the transcription factor Sp1 is acetylated in response to oxidative stress in neurons. Histone deacetylase (HDAC) inhibitors augment Sp1 acetylation, Sp1 DNA binding, and Sp1-dependent gene expression and confer resistance to oxidative stress-induced death <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> . Sp1 activation is necessary for the protective effects of HDAC inhibitors. Together, these results demonstrate that HDAC inhibitors inhibit oxidative death independent of polyglutamine expansions by activating an Sp1-dependent adaptive response. </jats:p>

収録刊行物

被引用文献 (4)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ