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@ARTICLE{Schuetzmann:141106,
      author       = {D. Schuetzmann and C. Walter and B. van Riel and S.
                      Kruse$^*$ and T. König and T. Erdmann and A. Tönges and E.
                      Bindels and A. Weilemann and C. Gebhard and K. Wethmar and
                      C. Perrod and J. Minderjahn and M. Rehli and R. Delwel and
                      G. Lenz and S. Gröschel and M. Dugas and F. Rosenbauer},
      title        = {{T}emporal auto-regulation during human {PU}.1 locus
                      {S}ub{TAD} formation.},
      journal      = {Blood},
      volume       = {132},
      number       = {22},
      issn         = {0006-4971},
      address      = {Stanford, Calif.},
      publisher    = {HighWire Press},
      reportid     = {DKFZ-2018-01640},
      pages        = {2643-2655},
      year         = {2018},
      abstract     = {Epigenetic control of gene expression occurs within
                      discrete spatial chromosomal units called topologically
                      associating domains (TADs), but the exact spatial
                      requirements of most genes are unknown; this is of
                      particular interest for genes involved in cancer. We
                      therefore applied high-resolution chromosomal conformation
                      capture-sequencing to map the three-dimensional (3D)
                      organization of the human locus encoding the key myeloid
                      transcription factor PU.1 in healthy monocytes and acute
                      myeloid leukemia (AML) cells. We identified a dynamic ~75kb
                      unit (SubTAD) as the genomic region in which spatial
                      interactions between PU.1 gene regulatory elements occur
                      during myeloid differentiation and are interrupted in AML.
                      Within this SubTAD, proper initiation of the spatial
                      chromosomal interactions requires PU.1 auto-regulation and
                      recruitment of the chromatin-adaptor protein LDB1 (LIM
                      domain-binding protein 1). However, once these spatial
                      interactions have occurred, LDB1 stabilizes them
                      independently of PU.1 auto-regulation. Thus, our data
                      support that PU.1 auto-regulates its expression in a
                      hit-and-run manner by initiating stable chromosomal loops
                      that result in a transcriptionally active chromatin
                      architecture.},
      cin          = {G240 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)G240-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30315124},
      doi          = {10.1182/blood-2018-02-834721},
      url          = {https://inrepo02.dkfz.de/record/141106},
}