Relationship between Methyl CpG Binding Protein 2 and JC Viral Proteins

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Author(s)

    • Takahashi Kenta Takahashi Kenta
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine|Division of Molecular Pathobiology, Research Center for Zoonosis Control, Hokkaido University
    • Kimura Taichi [他] Tanaka Shinya
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine|Department of Translational Pathology, Hokkaido University Graduate School of Medicine
    • Orba Yasuko
    • Division of Molecular Pathobiology, Research Center for Zoonosis Control, Hokkaido University
    • Kimura Taichi
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine
    • Wang Lei
    • Department of Translational Pathology, Hokkaido University Graduate School of Medicine
    • Kohsaka Shinji
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine
    • Tsuda Masumi
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine
    • Tanino Mishie
    • Department of Cancer Pathology, Hokkaido University Graduate School of Medicine
    • Nishihara Hiroshi
    • Department of Translational Pathology, Hokkaido University Graduate School of Medicine
    • Nagashima Kazuo
    • Department of Pathology, Sapporo Higashi-Tokushukai Hospital|Department of Cancer Pathology, Hokkaido University Graduate School of Medicine

Abstract

JC virus (JCV) is a causative agent of progressive multifocal leukoencephalopathy (PML). Methyl CpG binding protein 2 (MeCP2) is a transcriptional control nuclear protein that is abundantly expressed in neurons. We previously observed that the MeCP2 protein is expressed in JCV large T antigen (TAg)-expressing glial cells in PML brains. To investigate the relationship between MeCP2 and JCV TAg, we examined the promoter activity and mRNA and protein expression levels of MeCP2 in JCV TAg-expressing cells. We found that JCV TAg enhances the promoter activity of MeCP2, but does not enhance the mRNA and protein levels of MeCP2. These results suggest that post-transcriptional mechanisms may play a role in MeCP2 expression.

Journal

  • Japanese Journal of Infectious Diseases

    Japanese Journal of Infectious Diseases 66(2), 126-132, 2013

    National Institute of Infectious Diseases, Japanese Journal of Infectious Diseases Editorial Committee

Codes

  • NII Article ID (NAID)
    130003381654
  • NII NACSIS-CAT ID (NCID)
    AA1132885X
  • Text Lang
    ENG
  • ISSN
    1344-6304
  • NDL Article ID
    024360165
  • NDL Call No.
    Z53-C450
  • Data Source
    NDL  J-STAGE 
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