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@ARTICLE{Toda:257694,
      author       = {Toda, Tomohisa and Hsu, Jonathan Y and Linker, Sara B and
                      Hu, Lauren and Schafer, Simon T and Mertens, Jerome and
                      Jacinto, Filipe V and Hetzer, Martin W and Gage, Fred H},
      title        = {{N}up153 {I}nteracts with {S}ox2 to {E}nable {B}imodal
                      {G}ene {R}egulation and {M}aintenance of {N}eural
                      {P}rogenitor {C}ells.},
      journal      = {Cell stem cell},
      volume       = {21},
      number       = {5},
      issn         = {1934-5909},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-00491},
      pages        = {618 - 634.e7},
      year         = {2017},
      abstract     = {Neural progenitor cells (NeuPCs) possess a unique nuclear
                      architecture that changes during differentiation.
                      Nucleoporins are linked with cell-type-specific gene
                      regulation, coupling physical changes in nuclear structure
                      to transcriptional output; but, whether and how they
                      coordinate with key fate-determining transcription factors
                      is unclear. Here we show that the nucleoporin Nup153
                      interacts with Sox2 in adult NeuPCs, where it is
                      indispensable for their maintenance and controls neuronal
                      differentiation. Genome-wide analyses show that Nup153 and
                      Sox2 bind and co-regulate hundreds of genes. Binding of
                      Nup153 to gene promoters or transcriptional end sites
                      correlates with increased or decreased gene expression,
                      respectively, and inhibiting Nup153 expression alters open
                      chromatin configurations at its target genes, disrupts
                      genomic localization of Sox2, and promotes differentiation
                      in vitro and a gliogenic fate switch in vivo. Together,
                      these findings reveal that nuclear structural proteins may
                      exert bimodal transcriptional effects to control cell fate.},
      keywords     = {Animals / Chromatin: metabolism / Gene Expression
                      Regulation / Genome / Mice / Neural Stem Cells: metabolism /
                      Neurogenesis: genetics / Nuclear Pore Complex Proteins:
                      metabolism / Protein Binding / SOXB1 Transcription Factors:
                      metabolism / Transcription, Genetic / Nup153 (Other) / Sox2
                      (Other) / adult neurogenesis (Other) / bimodal gene
                      regulation (Other) / cell fate (Other) / key transcription
                      factors (Other) / neural differentiation (Other) / neural
                      progenitor cells (Other) / nucleoporins (Other) / spatial
                      transcriptional regulation (Other) / Chromatin (NLM
                      Chemicals) / Nuclear Pore Complex Proteins (NLM Chemicals) /
                      Nup153 protein, mouse (NLM Chemicals) / SOXB1 Transcription
                      Factors (NLM Chemicals)},
      ddc          = {570},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28919367},
      doi          = {10.1016/j.stem.2017.08.012},
      url          = {https://pub.dzne.de/record/257694},
}