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@ARTICLE{PierzynskaMach:285674,
      author       = {A. Pierzynska-Mach and C. Czada and C. Vogel and E. Gwosch
                      and X. Osswald and D. Bartoschek and A. Diaspro and F.
                      Kappes and E. Ferrando-May$^*$},
      title        = {{DEK} oncoprotein participates in heterochromatin
                      replication via {SUMO}-dependent nuclear bodies.},
      journal      = {Journal of cell science},
      volume       = {136},
      number       = {23},
      issn         = {0370-2952},
      address      = {Cambridge},
      publisher    = {Company of Biologists Limited},
      reportid     = {DKFZ-2023-02496},
      pages        = {jcs261329},
      year         = {2023},
      note         = {#LA:W650# / 2023 Dec 1;136(23):jcs261329},
      abstract     = {The correct inheritance of chromatin structure is key for
                      maintaining genome function and cell identity and preventing
                      cellular transformation. DEK, a conserved non-histone
                      chromatin protein, has recognized tumor-promoting
                      properties, its overexpression being associated with poor
                      prognosis in various cancer types. At the cellular level,
                      DEK displays pleiotropic functions, influencing
                      differentiation, apoptosis, and stemness, but a
                      characteristic oncogenic mechanism has remained elusive.
                      Here we report the identification of DEK bodies, focal
                      assemblies of DEK regularly occurring at specific, yet
                      unidentified sites of heterochromatin replication
                      exclusively in late S-phase. In these bodies, DEK localizes
                      in direct proximity to active replisomes in agreement with a
                      function in the early maturation of heterochromatin. A
                      high-throughput siRNA screen, supported by mutational and
                      biochemical analyses, identifies SUMO as one regulator of
                      DEK body formation, linking DEK to the complex SUMO protein
                      network that controls chromatin states and cell fate. This
                      work combines and refines our previous data on DEK as a
                      factor essential for heterochromatin integrity and
                      facilitating replication under stress and delineates an
                      avenue of further study for unraveling DEK´s contribution
                      to cancer development.},
      keywords     = {Breast cancer (Other) / Histone modification (Other) /
                      Oncogene (Other) / Replication stress (Other) / SiRNA screen
                      (Other) / Superresolution microscopy (Other)},
      cin          = {W650},
      ddc          = {570},
      cid          = {I:(DE-He78)W650-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37997922},
      doi          = {10.1242/jcs.261329},
      url          = {https://inrepo02.dkfz.de/record/285674},
}