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@ARTICLE{Pajtler:144769,
      author       = {K. Pajtler$^*$ and Y. Wei and K. Okonechnikov$^*$ and P. B.
                      G. Silva$^*$ and M. Vouri$^*$ and L. Zhang and S.
                      Brabetz$^*$ and L. Sieber$^*$ and M. Gulley and M.
                      Mauermann$^*$ and T. Wedig$^*$ and N. Mack$^*$ and Y.
                      Imamura Kawasawa and T. Sharma$^*$ and M. Zuckermann$^*$ and
                      F. Andreiuolo and E. Holland and K. Maass$^*$ and H.
                      Körkel-Qu$^*$ and H.-K. Liu$^*$ and F. Sahm$^*$ and D.
                      Capper$^*$ and J. Bunt and L. J. Richards and D. T. W.
                      Jones$^*$ and A. Korshunov$^*$ and L. Chavez$^*$ and P.
                      Lichter$^*$ and M. Hoshino and S. Pfister$^*$ and M.
                      Kool$^*$ and W. Li and D. Kawauchi$^*$},
      title        = {{YAP}1 subgroup supratentorial ependymoma requires {TEAD}
                      and nuclear factor {I}-mediated transcriptional programmes
                      for tumorigenesis.},
      journal      = {Nature Communications},
      volume       = {10},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2019-02201},
      pages        = {3914},
      year         = {2019},
      abstract     = {YAP1 fusion-positive supratentorial ependymomas
                      predominantly occur in infants, but the molecular mechanisms
                      of oncogenesis are unknown. Here we show YAP1-MAMLD1 fusions
                      are sufficient to drive malignant transformation in mice,
                      and the resulting tumors share histo-molecular
                      characteristics of human ependymomas. Nuclear localization
                      of YAP1-MAMLD1 protein is mediated by MAMLD1 and independent
                      of YAP1-Ser127 phosphorylation. Chromatin
                      immunoprecipitation-sequencing analyses of human
                      YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and
                      TEAD transcription factor binding site motifs in YAP1-bound
                      regulatory elements, suggesting a role for these
                      transcription factors in YAP1-MAMLD1-driven tumorigenesis.
                      Mutation of the TEAD binding site in the YAP1 fusion or
                      repression of NFI targets prevents tumor induction in mice.
                      Together, these results demonstrate that the YAP1-MAMLD1
                      fusion functions as an oncogenic driver of ependymoma
                      through recruitment of TEADs and NFIs, indicating a
                      rationale for preclinical studies to block the interaction
                      between YAP1 fusions and NFI and TEAD transcription
                      factors.},
      cin          = {B062 / B360 / A240 / B300 / B060},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B360-20160331 /
                      I:(DE-He78)A240-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)B060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31477715},
      pmc          = {pmc:PMC6718408},
      doi          = {10.1038/s41467-019-11884-5},
      url          = {https://inrepo02.dkfz.de/record/144769},
}