Cytoplasmic protein aggregates interfere with nucleocytoplasmic transport of protein and RNA

  • Andreas C. Woerner
    Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Frédéric Frottin
    Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Daniel Hornburg
    Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Li R. Feng
    Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Felix Meissner
    Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Maria Patra
    Neurobiochemistry, Adolf Butenandt Institute, Ludwig Maximilians University, Schillerstr. 44, D-80336 Munich, Germany.
  • Jörg Tatzelt
    Neurobiochemistry, Adolf Butenandt Institute, Ludwig Maximilians University, Schillerstr. 44, D-80336 Munich, Germany.
  • Matthias Mann
    Department of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Konstanze F. Winklhofer
    Neurobiochemistry, Adolf Butenandt Institute, Ludwig Maximilians University, Schillerstr. 44, D-80336 Munich, Germany.
  • F. Ulrich Hartl
    Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.
  • Mark S. Hipp
    Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany.

抄録

<jats:title>Location, location, location</jats:title> <jats:p> Aggregates of certain disease-associated proteins are involved in neurodegeneration. Woerner <jats:italic>et al.</jats:italic> now show that the exact location of these aggregates in the cell may be the key to their pathology (see the Perspective by Da Cruz and Cleveland). An artificial aggregate-prone protein caused problems when expressed in the cytoplasm but not when expressed in the nucleus. Cytoplasmic aggregates interfered with nucleocytoplasmic import and export. Perhaps if we can shunt pathological aggregates to the nucleus in the future, we will be able to ameliorate some forms of degenerative disease. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6269" page="173" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad2033">173</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6269" page="125" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad9872">125</jats:related-article> </jats:p>

収録刊行物

  • Science

    Science 351 (6269), 173-176, 2016-01-08

    American Association for the Advancement of Science (AAAS)

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