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@ARTICLE{Lafarga:143051,
      author       = {V. Lafarga$^*$ and H.-M. Sung$^*$ and K. Haneke$^*$ and L.
                      Roessig$^*$ and A.-L. Pauleau and M. Bruer$^*$ and S.
                      Rodriguez-Acebes and A. J. Lopez-Contreras and O. J. Gruss
                      and S. Erhardt and J. Mendez and O. Fernandez-Capetillo and
                      G. Stoecklin$^*$},
      title        = {{TIAR} marks nuclear {G}2/{M} transition granules and
                      restricts {CDK}1 activity under replication stress.},
      journal      = {EMBO reports},
      volume       = {20},
      number       = {1},
      issn         = {1469-3178},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2019-00670},
      pages        = {e46224},
      year         = {2019},
      note         = {DKFZ-ZMBH-Alliance},
      abstract     = {The G2/M checkpoint coordinates DNA replication with
                      mitosis and thereby prevents chromosome segregation in the
                      presence of unreplicated or damaged DNA Here, we show that
                      the RNA-binding protein TIAR is essential for the G2/M
                      checkpoint and that TIAR accumulates in nuclear foci in late
                      G2 and prophase in cells suffering from replication stress.
                      These foci, which we named G2/M transition granules (GMGs),
                      occur at low levels in normally cycling cells and are
                      strongly induced by replication stress. In addition to
                      replication stress response proteins, GMGs contain factors
                      involved in RNA metabolism as well as CDK1. Depletion of
                      TIAR accelerates mitotic entry and leads to chromosomal
                      instability in response to replication stress, in a manner
                      that can be alleviated by the concomitant depletion of
                      Cdc25B or inhibition of CDK1. Since TIAR retains CDK1 in
                      GMGs and attenuates CDK1 activity, we propose that the
                      assembly of GMGs may represent a so far unrecognized
                      mechanism that contributes to the activation of the G2/M
                      checkpoint in mammalian cells.},
      cin          = {A200},
      ddc          = {570},
      cid          = {I:(DE-He78)A200-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30538118},
      pmc          = {pmc:PMC6322364},
      doi          = {10.15252/embr.201846224},
      url          = {https://inrepo02.dkfz.de/record/143051},
}