@article{11067,
  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.},
  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.},
  issn         = {1934-5909},
  journal      = {Cell Stem Cell},
  keywords     = {Cell Biology, Genetics, Molecular Medicine},
  number       = {5},
  pages        = {618--634.e7},
  publisher    = {Elsevier},
  title        = {{Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells}},
  doi          = {10.1016/j.stem.2017.08.012},
  volume       = {21},
  year         = {2017},
}

@article{7141,
  author       = {Rolando, Chiara and Erni, Andrea and Grison, Alice and Beattie, Robert J and Engler, Anna and Gokhale, Paul J. and Milo, Marta and Wegleiter, Thomas and Jessberger, Sebastian and Taylor, Verdon},
  issn         = {1934-5909},
  journal      = {Cell Stem Cell},
  number       = {5},
  pages        = {653--662},
  publisher    = {Elsevier},
  title        = {{Multipotency of adult hippocampal NSCs in vivo is restricted by Drosha/NFIB}},
  doi          = {10.1016/j.stem.2016.07.003},
  volume       = {19},
  year         = {2016},
}

@article{11079,
  abstract     = {Aging is a major risk factor for many human diseases, and in vitro generation of human neurons is an attractive approach for modeling aging-related brain disorders. However, modeling aging in differentiated human neurons has proved challenging. We generated neurons from human donors across a broad range of ages, either by iPSC-based reprogramming and differentiation or by direct conversion into induced neurons (iNs). While iPSCs and derived neurons did not retain aging-associated gene signatures, iNs displayed age-specific transcriptional profiles and revealed age-associated decreases in the nuclear transport receptor RanBP17. We detected an age-dependent loss of nucleocytoplasmic compartmentalization (NCC) in donor fibroblasts and corresponding iNs and found that reduced RanBP17 impaired NCC in young cells, while iPSC rejuvenation restored NCC in aged cells. These results show that iNs retain important aging-related signatures, thus allowing modeling of the aging process in vitro, and they identify impaired NCC as an important factor in human aging.},
  author       = {Mertens, Jerome and Paquola, Apuã C.M. and Ku, Manching and Hatch, Emily and Böhnke, Lena and Ladjevardi, Shauheen and McGrath, Sean and Campbell, Benjamin and Lee, Hyungjun and Herdy, Joseph R. and Gonçalves, J. Tiago and Toda, Tomohisa and Kim, Yongsung and Winkler, Jürgen and Yao, Jun and HETZER, Martin W and Gage, Fred H.},
  issn         = {1934-5909},
  journal      = {Cell Stem Cell},
  keywords     = {Cell Biology, Genetics, Molecular Medicine},
  number       = {6},
  pages        = {705--718},
  publisher    = {Elsevier},
  title        = {{Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects}},
  doi          = {10.1016/j.stem.2015.09.001},
  volume       = {17},
  year         = {2015},
}