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@ARTICLE{Szulzewsky:157169,
      author       = {F. Szulzewsky and S. Arora and P. Hoellerbauer and C. King
                      and E. Nathan and M. Chan and P. J. Cimino and T. Ozawa and
                      D. Kawauchi$^*$ and K. W. Pajtler$^*$ and R. J. Gilbertson
                      and P. J. Paddison and V. Vasioukhin and T. S. Gujral and E.
                      C. Holland},
      title        = {{C}omparison of tumor-associated {YAP}1 fusions identifies
                      a recurrent set of functions critical for oncogenesis.},
      journal      = {Genes $\&$ development},
      volume       = {34},
      number       = {15-16},
      issn         = {1549-5477},
      address      = {Cold Spring Harbor, NY},
      publisher    = {Laboratory Press},
      reportid     = {DKFZ-2020-01449},
      pages        = {1051-1064},
      year         = {2020},
      note         = {Volume 34, Issue 15-16, 1 August 2020, Pages 1051-1064},
      abstract     = {YAP1 is a transcriptional coactivator and the principal
                      effector of the Hippo signaling pathway, which is causally
                      implicated in human cancer. Several YAP1 gene fusions have
                      been identified in various human cancers and identifying the
                      essential components of this family of gene fusions has
                      significant therapeutic value. Here, we show that the YAP1
                      gene fusions YAP1-MAMLD1, YAP1-FAM118B, YAP1-TFE3, and
                      YAP1-SS18 are oncogenic in mice. Using reporter assays,
                      RNA-seq, ChIP-seq, and loss-of-function mutations, we can
                      show that all of these YAP1 fusion proteins exert
                      TEAD-dependent YAP activity, while some also exert activity
                      of the C'-terminal fusion partner. The YAP activity of the
                      different YAP1 fusions is resistant to negative Hippo
                      pathway regulation due to constitutive nuclear localization
                      and resistance to degradation of the YAP1 fusion proteins.
                      Genetic disruption of the TEAD-binding domain of these
                      oncogenic YAP1 fusions is sufficient to inhibit tumor
                      formation in vivo, while pharmacological inhibition of the
                      YAP1-TEAD interaction inhibits the growth of YAP1
                      fusion-expressing cell lines in vitro. These results
                      highlight TEAD-dependent YAP activity found in these gene
                      fusions as critical for oncogenesis and implicate these YAP
                      functions as potential therapeutic targets in YAP1
                      fusion-positive tumors.},
      cin          = {B062},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32675324},
      doi          = {10.1101/gad.338681.120},
      url          = {https://inrepo02.dkfz.de/record/157169},
}