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      author       = {R. Kupp and L. Ruff and S. Terranova and E. Nathan and S.
                      Ballereau and R. Stark and C. Sekhar Reddy Chilamakuri and
                      N. Hoffmann and K. Wickham-Rahrmann and M. Widdess and A.
                      Arabzade and Y. Zhao and S. Varadharajan and T. Zheng$^*$
                      and M. K. Murugesan and S. Pfister$^*$ and D. Kawauchi and
                      K. W. Pajtler$^*$ and B. Deneen and S. C. Mack and K. E.
                      Masih and B. E. Gryder and J. Khan and R. J. Gilbertson},
      title        = {{ZFTA}-translocations constitute ependymoma chromatin
                      remodeling and transcription factors.},
      journal      = {Cancer discovery},
      volume       = {11},
      number       = {9},
      issn         = {2159-8290},
      address      = {Philadelphia, Pa.},
      reportid     = {DKFZ-2021-00678},
      pages        = {2216-2229},
      year         = {2021},
      note         = {2021 Sep;11(9):2216-2229},
      abstract     = {ZFTA (C11orf95)-a gene of unknown function-partners with a
                      variety of transcriptional co-activators in translocations
                      that drive supratentorial ependymoma, a frequently lethal
                      brain tumor. Understanding the function of ZFTA is key to
                      developing therapies that inhibit these fusion proteins.
                      Here, using a combination of transcriptomics, chromatin
                      immunoprecipitation-sequencing, and proteomics, we
                      interrogated a series of deletion-mutant genes to identify a
                      tri-partite transformation mechanism of ZFTA-containing
                      fusions, including: spontaneous nuclear translocation,
                      extensive chromatin binding, and SWI/SNF, SAGA and
                      NuA4/Tip60 HAT chromatin modifier complex recruitment.
                      Thereby, ZFTA tethers fusion proteins across the genome,
                      modifying chromatin to an active state, and enabling its
                      partner transcriptional co-activators to promote promiscuous
                      expression of a transforming transcriptome. Using mouse
                      models, we validate further those elements of ZFTA-fusion
                      proteins that are critical for transformation-including ZFTA
                      zinc fingers and partner gene transactivation
                      domains-thereby unmasking vulnerabilities for therapeutic
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33741711},
      doi          = {10.1158/2159-8290.CD-20-1052},
      url          = {https://inrepo02.dkfz.de/record/168090},