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@ARTICLE{Gozdecka:135956,
      author       = {M. Gozdecka and E. Meduri and M. Mazan and K. Tzelepis and
                      M. Dudek and A. J. Knights and M. Pardo and L. Yu and J. S.
                      Choudhary and E. Metzakopian and V. Iyer and H. Yun and N.
                      Park and I. Varela and R. Bautista and G. Collord and O.
                      Dovey and D. A. Garyfallos and E. De Braekeleer and S. Kondo
                      and J. Cooper and B. Göttgens and L. Bullinger and P. A.
                      Northcott$^*$ and D. Adams and G. S. Vassiliou and B. J. P.
                      Huntly},
      title        = {{UTX}-mediated enhancer and chromatin remodeling suppresses
                      myeloid leukemogenesis through noncatalytic inverse
                      regulation of {ETS} and {GATA} programs.},
      journal      = {Nature genetics},
      volume       = {50},
      number       = {6},
      issn         = {1546-1718},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DKFZ-2018-00693},
      pages        = {883 - 894},
      year         = {2018},
      abstract     = {The histone H3 Lys27-specific demethylase UTX (or KDM6A) is
                      targeted by loss-of-function mutations in multiple cancers.
                      Here, we demonstrate that UTX suppresses myeloid
                      leukemogenesis through noncatalytic functions, a property
                      shared with its catalytically inactive Y-chromosome paralog,
                      UTY (or KDM6C). In keeping with this, we demonstrate
                      concomitant loss/mutation of KDM6A (UTX) and UTY in multiple
                      human cancers. Mechanistically, global genomic profiling
                      showed only minor changes in H3K27me3 but significant and
                      bidirectional alterations in H3K27ac and chromatin
                      accessibility; a predominant loss of H3K4me1 modifications;
                      alterations in ETS and GATA-factor binding; and altered gene
                      expression after Utx loss. By integrating proteomic and
                      genomic analyses, we link these changes to UTX regulation of
                      ATP-dependent chromatin remodeling, coordination of the
                      COMPASS complex and enhanced pioneering activity of ETS
                      factors during evolution to AML. Collectively, our findings
                      identify a dual role for UTX in suppressing acute myeloid
                      leukemia via repression of oncogenic ETS and upregulation of
                      tumor-suppressive GATA programs.},
      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:29736013},
      doi          = {10.1038/s41588-018-0114-z},
      url          = {https://inrepo02.dkfz.de/record/135956},
}