Sheng Zhang

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Inactivation of Drosophila Huntingtin affects long-term adult functioning and the pathogenesis of a Huntington's disease model
    Sheng Zhang
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Dis Model Mech 2:247-66. 2009
  2. pmc A genomewide RNA interference screen for modifiers of aggregates formation by mutant Huntingtin in Drosophila
    Sheng Zhang
    Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genetics 184:1165-79. 2010
  3. ncbi request reprint Drosophila atrophin homolog functions as a transcriptional corepressor in multiple developmental processes
    Sheng Zhang
    Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06535, USA
    Cell 108:45-56. 2002

Detail Information

Publications3

  1. pmc Inactivation of Drosophila Huntingtin affects long-term adult functioning and the pathogenesis of a Huntington's disease model
    Sheng Zhang
    Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
    Dis Model Mech 2:247-66. 2009
    ....
  2. pmc A genomewide RNA interference screen for modifiers of aggregates formation by mutant Huntingtin in Drosophila
    Sheng Zhang
    Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genetics 184:1165-79. 2010
    ..Thus, other aggregates regulators isolated in our screen may identify additional genes involved in the protein-folding pathway and neurotoxicity...
  3. ncbi request reprint Drosophila atrophin homolog functions as a transcriptional corepressor in multiple developmental processes
    Sheng Zhang
    Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06535, USA
    Cell 108:45-56. 2002
    ..We propose that Atrophin proteins function as versatile transcriptional corepressors and discuss a model that deregulation of transcription may contribute to the pathogenesis of neurodegeneration...