% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Wang:169864,
      author       = {Y. Wang and B. Li and L. Dong and W. Duan and A.
                      Neuerburg$^*$ and H. Zhang and X. Jiang and R. Shao and Y.
                      Zhu and D. Bock$^*$ and E. Liu and H. Wang and Y. Zhang and
                      Y. Dai and H. Yang and Y. Wang},
      title        = {{I}mpaired generation of mature neurons due to extended
                      expression of {T}lx by repressing {S}ox2 transcriptional
                      activity.},
      journal      = {Stem cells},
      volume       = {39},
      number       = {11},
      issn         = {1066-5099},
      address      = {Hoboken, NJ},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2021-01598},
      pages        = {1520-1531},
      year         = {2021},
      note         = {Neuerburg, Bock: Division of Molecular Biology of the Cell
                      I, German Cancer Research Center (DKFZ) /2021
                      Nov;39(11):1520-1531 /DKFZ-ZMBH Alliance},
      abstract     = {As a master regulator of the dynamic process of adult
                      neurogenesis, timely expression and regulation of the orphan
                      nuclear receptor Tailless (Tlx) is essential. However, there
                      is no study yet to directly investigate the essential role
                      of precise spatiotemporal expressed Tlx. Here, we generated
                      a conditional gain of Tlx expression transgenic mouse model,
                      which allowed the extended Tlx expression in neural stem
                      cells (NSCs) and their progeny by mating with a TlxCreERT2
                      mouse line. We demonstrate that extended expression of Tlx
                      induced the impaired generation of mature neurons in adult
                      subventricular zone and subgranular zone. Furthermore, we
                      elucidated for the first time that this mutation decreased
                      the endogenous expression of Sox2 by directly binding to its
                      promoter. Restoration experiments further confirmed that
                      Sox2 partially rescued these neuron maturation defects.
                      Together, these findings not only highlight the importance
                      of shutting-off Tlx on time in controlling NSC behavior, but
                      also provide insights for further understanding adult
                      neurogenesis and developing treatment strategies for
                      neurological disorders.},
      keywords     = {Sox2 (Other) / Tlx (Other) / adult neurogenesis (Other) /
                      neural differentiation (Other) / neural stem cell (Other)},
      cin          = {A240 / W190},
      ddc          = {610},
      cid          = {I:(DE-He78)A240-20160331 / I:(DE-He78)W190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34269496},
      doi          = {10.1002/stem.3435},
      url          = {https://inrepo02.dkfz.de/record/169864},
}