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@ARTICLE{Grkalar:301336,
      author       = {H. K. Gürkaşlar$^*$ and I. Hoffmann$^*$},
      title        = {{B}inding of {CEP}152 to {PLK}4 stimulates kinase activity
                      to promote centriole assembly.},
      journal      = {Molecular biology of the cell},
      volume       = {36},
      number       = {7},
      issn         = {1059-1524},
      address      = {Bethesda, Md.},
      publisher    = {American Society for Cell Biology},
      reportid     = {DKFZ-2025-01002},
      pages        = {br17},
      year         = {2025},
      note         = {#EA:D345#LA:D345# / 2025 Jul 1;36(7):br17},
      abstract     = {Centriole duplication is regulated by polo-like kinase 4
                      (PLK4) and several conserved initiator proteins. The precise
                      timing and regulation of PLK4 activation are critical for
                      ensuring that centriole duplication occurs only once per
                      cell cycle. While significant progress has been made in
                      understanding how PLK4 is activated, many aspects remain
                      unclear. Here, we show how CEP152 contributes to the
                      activation of PLK4. We utilize human cell lines that have
                      been genetically engineered to rapidly degrade CEP152. Upon
                      degradation of CEP152, localization of PLK4 at the proximal
                      end of the centriole is disrupted. We show that binding of
                      CEP152 N-terminal part to PLK4 increases phosphorylation and
                      kinase activation. CEP152 controls the localization and
                      levels of phosphorylated PLK4 at the proximal end of the
                      centriole. CEP152 binding to PLK4 leads to phosphorylation
                      and activation of PLK4 which might stabilize PLK4 dimer
                      formation, thus allowing autophosphorylation. We propose
                      that CEP152 activates PLK4 to ensure proper centriole
                      duplication at the onset of S-phase.},
      cin          = {D345},
      ddc          = {570},
      cid          = {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:40372713},
      doi          = {10.1091/mbc.E24-12-0581},
      url          = {https://inrepo02.dkfz.de/record/301336},
}