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@ARTICLE{Lupo:134832,
      author       = {G. Lupo and P. S. Nisi and P. Esteve and Y.-L. Paul and C.
                      L. Novo and B. Sidders and M. A. Khan$^*$ and S. Biagioni
                      and H.-K. Liu$^*$ and P. Bovolenta and E. Cacci and P. J.
                      Rugg-Gunn},
      title        = {{M}olecular profiling of aged neural progenitors identifies
                      {D}bx2 as a candidate regulator of age-associated neurogenic
                      decline.},
      journal      = {Aging cell},
      volume       = {17},
      number       = {3},
      issn         = {1474-9718},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2018-00622},
      pages        = {e12745 -},
      year         = {2018},
      note         = {DKFZ-ZMBH-Allianz},
      abstract     = {Adult neurogenesis declines with aging due to the depletion
                      and functional impairment of neural stem/progenitor cells
                      (NSPCs). An improved understanding of the underlying
                      mechanisms that drive age-associated neurogenic deficiency
                      could lead to the development of strategies to alleviate
                      cognitive impairment and facilitate neuroregeneration. An
                      essential step towards this aim is to investigate the
                      molecular changes that occur in NSPC aging on a genomewide
                      scale. In this study, we compare the transcriptional,
                      histone methylation and DNA methylation signatures of NSPCs
                      derived from the subventricular zone (SVZ) of young adult
                      (3 months old) and aged (18 months old) mice.
                      Surprisingly, the transcriptional and epigenomic profiles of
                      SVZ-derived NSPCs are largely unchanged in aged cells.
                      Despite the global similarities, we detect robust
                      age-dependent changes at several hundred genes and
                      regulatory elements, thereby identifying putative regulators
                      of neurogenic decline. Within this list, the homeobox gene
                      Dbx2 is upregulated in vitro and in vivo, and its promoter
                      region has altered histone and DNA methylation levels, in
                      aged NSPCs. Using functional in vitro assays, we show that
                      elevated Dbx2 expression in young adult NSPCs promotes
                      age-related phenotypes, including the reduced proliferation
                      of NSPC cultures and the altered transcript levels of
                      age-associated regulators of NSPC proliferation and
                      differentiation. Depleting Dbx2 in aged NSPCs caused the
                      reverse gene expression changes. Taken together, these
                      results provide new insights into the molecular programmes
                      that are affected during mouse NSPC aging, and uncover a new
                      functional role for Dbx2 in promoting age-related neurogenic
                      decline.},
      cin          = {A240},
      ddc          = {610},
      cid          = {I:(DE-He78)A240-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29504228},
      pmc          = {pmc:PMC5946077},
      doi          = {10.1111/acel.12745},
      url          = {https://inrepo02.dkfz.de/record/134832},
}