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@ARTICLE{Li:276775,
      author       = {F. Li and E. Mladenov and Y. Sun and A. Soni and M.
                      Stuschke$^*$ and B. Timmermann$^*$ and G. Iliakis},
      title        = {{L}ow {CDK} {A}ctivity and {E}nhanced {D}egradation by
                      {APC}/{CCDH}1 {A}bolishes {C}t{IP} {A}ctivity and {A}lt-{EJ}
                      in {Q}uiescent {C}ells.},
      journal      = {Cells},
      volume       = {12},
      number       = {11},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2023-01156},
      pages        = {1530},
      year         = {2023},
      abstract     = {Alt-EJ is an error-prone DNA double-strand break (DSBs)
                      repair pathway coming to the fore when first-line repair
                      pathways, c-NHEJ and HR, are defective or fail. It is
                      thought to benefit from DNA end-resection-a process whereby
                      3' single-stranded DNA-tails are generated-initiated by the
                      CtIP/MRE11-RAD50-NBS1 (MRN) complex and extended by EXO1 or
                      the BLM/DNA2 complex. The connection between alt-EJ and
                      resection remains incompletely characterized. Alt-EJ depends
                      on the cell cycle phase, is at maximum in G2-phase,
                      substantially reduced in G1-phase and almost undetectable in
                      quiescent, G0-phase cells. The mechanism underpinning this
                      regulation remains uncharacterized. Here, we compare alt-EJ
                      in G1- and G0-phase cells exposed to ionizing radiation (IR)
                      and identify CtIP-dependent resection as the key regulator.
                      Low levels of CtIP in G1-phase cells allow modest resection
                      and alt-EJ, as compared to G2-phase cells. Strikingly, CtIP
                      is undetectable in G0-phase cells owing to APC/C-mediated
                      degradation. The suppression of CtIP degradation with
                      bortezomib or CDH1-depletion rescues CtIP and alt-EJ in
                      G0-phase cells. CtIP activation in G0-phase cells also
                      requires CDK-dependent phosphorylation by any available CDK
                      but is restricted to CDK4/6 at the early stages of the
                      normal cell cycle. We suggest that suppression of mutagenic
                      alt-EJ in G0-phase is a mechanism by which cells of higher
                      eukaryotes maintain genomic stability in a large fraction of
                      non-cycling cells in their organisms.},
      keywords     = {Phosphorylation / Nuclear Proteins: metabolism / DNA Repair
                      / DNA Breaks, Double-Stranded / Cell Cycle Checkpoints /
                      APC/C (Other) / CDKs (Other) / CtIP (Other) / DNA
                      end-resection (Other) / DNA repair (Other) / RPA (Other) /
                      alt-EJ (Other) / ionizing radiation (Other) / pulsed-field
                      gel electrophoresis (Other) / repair of DNA double-strand
                      breaks (Other) / Nuclear Proteins (NLM Chemicals)},
      cin          = {ED01},
      ddc          = {570},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37296650},
      pmc          = {pmc:PMC10252496},
      doi          = {10.3390/cells12111530},
      url          = {https://inrepo02.dkfz.de/record/276775},
}