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@ARTICLE{SchultzRogers:179097,
      author       = {L. E. Schultz-Rogers and M. L. Thayer and S. Kambakam and
                      W. A. Wierson and J. A. Helmer and M. D. Wishman and K. A.
                      Wall and J. L. Greig and J. L. Forsman and K. Puchhalapalli
                      and S. Nair and T. J. Weiss and J. M. Luiken and P. R.
                      Blackburn and S. C. Ekker and M. Kool$^*$ and M. McGrail},
      title        = {{R}bbp4 loss disrupts neural progenitor cell cycle
                      regulation independent of {R}b and leads to {T}p53
                      acetylation and apoptosis.},
      journal      = {Developmental dynamics},
      volume       = {251},
      number       = {8},
      issn         = {0002-9106},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2022-00462},
      pages        = {1267-1290},
      year         = {2022},
      note         = {2022 Aug;251(8):1267-1290},
      abstract     = {Retinoblastoma-binding protein 4 (Rbbp4) is a component of
                      transcription regulatory complexes that control cell cycle
                      gene expression. Previous work indicated Rbbp4 cooperates
                      with the Rb tumor suppressor to block cell cycle entry.
                      Here, we use genetic analysis to examine the interactions of
                      Rbbp4, Rb and Tp53 in zebrafish neural progenitor cell cycle
                      regulation and survival.Rbbp4 is upregulated across the
                      spectrum of human embryonal and glial brain cancers.
                      Transgenic rescue of rbbp4 mutant embryos shows Rbbp4 is
                      essential for zebrafish neurogenesis. Rbbp4 loss leads to
                      apoptosis and γ-H2AX in the developing brain that is
                      suppressed by tp53 knockdown or maternal zygotic deletion.
                      Mutant retinal neural precursors accumulate in M phase and
                      fail to initiate G0 gene expression. rbbp4; rb1 mutants show
                      an additive effect on the number of M phase cells. In rbbp4
                      mutants Tp53 acetylation is detected, however, Rbbp4
                      overexpression did not rescue DNA damage induced
                      apoptosis.Rbbp4 is necessary for neural progenitor cell
                      cycle progression and initiation of G0 independent of Rb.
                      Tp53-dependent apoptosis in the absence of Rbpb4 correlates
                      with Tp53 acetylation. Together these results suggest Rbbp4
                      is required for cell cycle exit and contributes to neural
                      progenitor survival through regulation of Tp53 acetylation.
                      This article is protected by copyright. All rights
                      reserved.},
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35266256},
      doi          = {10.1002/dvdy.467},
      url          = {https://inrepo02.dkfz.de/record/179097},
}