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@ARTICLE{Grossmann:289013,
      author       = {J. Grossmann$^*$ and A.-S. Kratz$^*$ and A. Kordonsky and
                      G. Prag and I. Hoffmann$^*$},
      title        = {{CRL}4{DCAF}1 ubiquitin ligase regulates {PLK}4 protein
                      levels to prevent premature centriole duplication.},
      journal      = {Life science alliance},
      volume       = {7},
      number       = {6},
      issn         = {2575-1077},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2024-00545},
      pages        = {e202402668 -},
      year         = {2024},
      note         = {#EA:F045#LA:F045# / NEU/ #EA:D345#LA:D345#},
      abstract     = {Centrioles play important roles in the assembly of
                      centrosomes and cilia. Centriole duplication occurs once per
                      cell cycle and is dependent on polo-like kinase 4 (PLK4). To
                      prevent centriole amplification, which is a hallmark of
                      cancer, PLK4 protein levels need to be tightly regulated.
                      Here, we show that the Cullin4A/B-DDB1-DCAF1, CRL4DCAF1, E3
                      ligase targets PLK4 for degradation in human cells. DCAF1
                      binds and ubiquitylates PLK4 in the G2 phase to prevent
                      premature centriole duplication in mitosis. In contrast to
                      the regulation of PLK4 by SCFβ-TrCP, the interaction
                      between PLK4 and DCAF1 is independent of PLK4 kinase
                      activity and mediated by polo-boxes 1 and 2 of PLK4,
                      suggesting that DCAF1 promotes PLK4 ubiquitylation
                      independently of β-TrCP. Thus, the SCFSlimb/β-TrCP
                      pathway, targeting PLK4 for ubiquitylation based on its
                      phosphorylation state and CRL4DCAF1, which ubiquitylates
                      PLK4 by binding to the conserved PB1-PB2 domain, appear to
                      be complementary ways to control PLK4 abundance to prevent
                      centriole overduplication.},
      cin          = {F045 / D345},
      ddc          = {570},
      cid          = {I:(DE-He78)F045-20160331 / I:(DE-He78)D345-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38490717},
      pmc          = {pmc:PMC10942865},
      doi          = {10.26508/lsa.202402668},
      url          = {https://inrepo02.dkfz.de/record/289013},
}