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@ARTICLE{Benabdallah:282958,
      author       = {N. S. Benabdallah$^*$ and V. Dalal$^*$ and R. W. Scott and
                      F. Marcous$^*$ and A. Sotiriou$^*$ and F. K. Kommoss$^*$ and
                      A. Pejkovska$^*$ and L. Gaspar$^*$ and L. Wagner$^*$ and F.
                      J. Sánchez-Rivera and M. Ta and S. Thornton and T. O.
                      Nielsen and T. M. Underhill and A. Banito$^*$},
      title        = {{A}berrant gene activation in synovial sarcoma relies on
                      {SSX} specificity and increased {PRC}1.1 stability.},
      journal      = {Nature structural $\&$ molecular biology},
      volume       = {30},
      number       = {11},
      issn         = {1545-9993},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2023-01910},
      pages        = {1640-1652},
      year         = {2023},
      note         = {#EA:B380#LA:B380# / 2023 Nov;30(11):1640-1652},
      abstract     = {The SS18-SSX fusion drives oncogenic transformation in
                      synovial sarcoma by bridging SS18, a member of the mSWI/SNF
                      (BAF) complex, to Polycomb repressive complex 1 (PRC1)
                      target genes. Here we show that the ability of SS18-SSX to
                      occupy H2AK119ub1-rich regions is an intrinsic property of
                      its SSX C terminus, which can be exploited by fusion to
                      transcriptional regulators beyond SS18. Accordingly,
                      SS18-SSX recruitment occurs in a manner that is independent
                      of the core components and catalytic activity of BAF.
                      Alternative SSX fusions are also recruited to
                      H2AK119ub1-rich chromatin and reproduce the expression
                      signatures of SS18-SSX by engaging with transcriptional
                      activators. Variant Polycomb repressive complex 1.1 (PRC1.1)
                      acts as the main depositor of H2AK119ub1 and is therefore
                      required for SS18-SSX occupancy. Importantly, the SSX C
                      terminus not only depends on H2AK119ub1 for localization,
                      but also further increases it by promoting PRC1.1 complex
                      stability. Consequently, high H2AK119ub1 levels are a
                      feature of murine and human synovial sarcomas. These results
                      uncover a critical role for SSX-C in mediating gene
                      deregulation in synovial sarcoma by providing specificity to
                      chromatin and further enabling oncofusion binding by
                      enhancing PRC1.1 stability and H2AK119ub1 deposition.},
      cin          = {B380},
      ddc          = {570},
      cid          = {I:(DE-He78)B380-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37735617},
      doi          = {10.1038/s41594-023-01096-3},
      url          = {https://inrepo02.dkfz.de/record/282958},
}