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@ARTICLE{Frhlich:811943,
      author       = {Fröhlich, Michael and Jaeger, Alexandra and Weiss, Dieter
                      G. and Kriehuber, Ralf},
      title        = {{I}nhibition of {BCL}-2 leads to increased apoptosis and
                      delayed neuronal differentiation in human {R}e{N}cell {VM}
                      cells in vitro},
      journal      = {International journal of developmental neuroscience},
      volume       = {48},
      issn         = {0736-5748},
      address      = {Oxford [u.a.]},
      publisher    = {Pergamon Press},
      reportid     = {FZJ-2016-04253},
      pages        = {9 - 17},
      year         = {2016},
      abstract     = {BCL-2 is a multifunctional protein involved in the
                      regulation of apoptosis, cell cycle progression and neural
                      developmental processes. Its function in the latter process
                      is not well understood and needs further elucidation.
                      Therefore, we characterized the protein expression kinetics
                      of BCL-2 and associated regulatory proteins of the intrinsic
                      apoptosis pathway during the process of neuronal
                      differentiation in ReNcell VM cells with and without
                      functional inhibition of BCL-2 by its competitive ligand
                      HA14-1. Inhibition of BCL-2 caused a diminished BCL-2
                      expression and higher levels of cleaved BAX, activated
                      Caspase-3 and cleaved PARP, all pro-apoptotic markers, when
                      compared with untreated differentiating cells. In parallel,
                      flow cytometric analysis of HA14-1-treated cells revealed a
                      delayed differentiation into HuC/D+ neuronal cells when
                      compared to untreated differentiating cells. In conclusion,
                      BCL-2 possess a protective function in fully differentiated
                      ReNcell VM cells. We propose that the pro-survival signaling
                      of BCL-2 is closely connected with its stimulatory effects
                      on neurogenesis of human neural progenitor cells.},
      cin          = {S-US},
      ddc          = {610},
      cid          = {I:(DE-Juel1)S-US-20090406},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000369679300002},
      doi          = {10.1016/j.ijdevneu.2015.10.004},
      url          = {https://juser.fz-juelich.de/record/811943},
}