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@ARTICLE{Ecker:157624,
      author       = {J. Ecker$^*$ and V. Thatikonda$^*$ and G. Sigismondo$^*$
                      and F. Selt$^*$ and G. Valinciute$^*$ and I. Oehme$^*$ and
                      C. Müller$^*$ and J. L. Buhl$^*$ and J. Ridinger$^*$ and D.
                      Usta$^*$ and N. Qin$^*$ and C. M. van Tilburg$^*$ and C.
                      Herold-Mende and M. Remke$^*$ and F. Sahm$^*$ and F.
                      Westermann$^*$ and M. Kool$^*$ and R. J. Wechsler-Reya and
                      L. Chavez and J. Krijgsveld$^*$ and N. Jäger$^*$ and S. M.
                      Pfister$^*$ and O. Witt$^*$ and T. Milde$^*$},
      title        = {{R}educed chromatin binding of {MYC} is a key effect of
                      {HDAC} inhibition in {MYC} amplified medulloblastoma.},
      journal      = {Neuro-Oncology},
      volume       = {23},
      number       = {2},
      issn         = {1523-5866},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2020-01721},
      pages        = {226-239},
      year         = {2021},
      note         = {#EA:B310#LA:B310#2021 Feb 25;23(2):226-239},
      abstract     = {The sensitivity of MYC amplified medulloblastoma to class I
                      HDAC inhibition has been shown previously, however
                      understanding the underlying molecular mechanism is crucial
                      for selection of effective HDAC inhibitors for clinical use.
                      The aim of this study was to investigate the direct
                      molecular interaction of MYC and the class I HDAC2, and the
                      impact of class I HDAC inhibition on MYC
                      function.Co-immunoprecipitation and mass spectrometry was
                      used to determine the co-localization of MYC and HDAC2.
                      ChIP-sequencing and gene expression profiling was used to
                      analyze the co- localization of MYC and HDAC2 on DNA and the
                      impact on transcriptional activity in primary tumors and a
                      MYC amplified cell line treated with the class I HDAC
                      inhibitor entinostat. The effect on MYC was investigated by
                      quantitative RT-PCR, Western blot and
                      immunofluorescence.HDAC2 is a cofactor of MYC in MYC
                      amplified medulloblastoma. The MYC-HDAC2 complex is bound to
                      genes defining the MYC-dependent transcriptional profile.
                      Class I HDAC inhibition leads to stabilization and reduced
                      DNA-binding of MYC protein inducing a down-regulation of MYC
                      activated genes (MAGs) and up-regulation of MYC repressed
                      genes (MRGs). MAGs and MRGs are characterized by opposing
                      biological functions and by distinct E-box distribution.Our
                      data elucidates the molecular interaction of MYC and HDAC2
                      and support a model in which inhibition of class I HDACs
                      directly targets MYC´s trans-activating and
                      trans-repressing function.},
      cin          = {B310 / HD01 / B062 / ED01 / B300 / B087 / B230},
      ddc          = {610},
      cid          = {I:(DE-He78)B310-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B062-20160331 / I:(DE-He78)ED01-20160331 /
                      I:(DE-He78)B300-20160331 / I:(DE-He78)B087-20160331 /
                      I:(DE-He78)B230-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32822486},
      doi          = {10.1093/neuonc/noaa191},
      url          = {https://inrepo02.dkfz.de/record/157624},
}