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@ARTICLE{Jaeger:129366,
      author       = {Jaeger, Alexandra and Baake, Jana and Weiss, Dieter G and
                      Kriehuber, Ralf},
      title        = {{G}lycogen synthase kinase-3beta regulates
                      differentiation-induced apoptosis of human neural progenitor
                      cells.},
      journal      = {International journal of developmental neuroscience},
      volume       = {31},
      number       = {1},
      issn         = {0736-5748},
      address      = {Oxford [u.a.]},
      publisher    = {Pergamon Press},
      reportid     = {FZJ-2013-00882},
      pages        = {61 - 68},
      year         = {2013},
      abstract     = {Glycogen synthase kinase-3beta is a multifunctional key
                      regulator enzyme in neural developmental processes and a
                      main component of the canonical Wnt signaling pathway. It is
                      already known that the Wnt-driven differentiation of neural
                      progenitor cells is accompanied by an increase of apoptosis
                      at which the pro-apoptotic function of GSK-3beta is still
                      discussed. The aim of the present study was to investigate
                      whether the phosphorylation level of GSK-3beta at serine 9
                      is the primary regulatory mechanism of
                      differentiation-induced apoptosis. Differentiating human
                      neural ReNcell VM progenitor cells were treated with the
                      specific GSK-3beta inhibitor SB216763 (10μM) and analyzed
                      in respect to the intrinsic apoptosis pathway regulation
                      using microscopy and protein expression analysis.
                      Differentiation of ReNcell VM cells was accompanied by cell
                      morphological changes, cytoskeleton rearrangement and
                      apoptosis increase. Treatment of differentiating cells with
                      SB216763 induced a significant dephosphorylation of
                      GSK-3beta at serine 9 accompanied by a significant decrease
                      of apoptosis of about $0.7±0.03\%$ and reduced activation
                      of caspase-3 as well as BAX and PARP cleavage during the
                      first 12h of differentiation compared to untreated,
                      differentiating cells. Dephosphorylation of GSK-3beta at
                      serine 9 appears not solely to be responsible for its
                      pro-apoptotic function, because we observed a decrease of
                      intrinsic apoptosis after treatment of the cells with the
                      specific GSK-3beta inhibitor SB216763. We assume that
                      GSK-3beta drives neural progenitor cell apoptosis by direct
                      interaction with pro-apoptotic BAX or by indirect influence
                      on the canonical Wnt/beta-catenin target gene
                      transcription.},
      cin          = {S-US},
      ddc          = {610},
      cid          = {I:(DE-Juel1)S-US-20090406},
      pnm          = {899 - ohne Topic (POF2-899)},
      pid          = {G:(DE-HGF)POF2-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23085082},
      UT           = {WOS:000313997300009},
      doi          = {10.1016/j.ijdevneu.2012.10.005},
      url          = {https://juser.fz-juelich.de/record/129366},
}