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@ARTICLE{Luo:276747,
      author       = {D. Luo and E. Mladenov and A. Soni and M. Stuschke$^*$ and
                      G. Iliakis},
      title        = {{T}he p38/{MK}2 {P}athway {F}unctions as {C}hk1-{B}ackup
                      {D}ownstream of {ATM}/{ATR} in {G}2-{C}heckpoint
                      {A}ctivation in {C}ells {E}xposed to {I}onizing {R}adiation},
      journal      = {Cells},
      volume       = {12},
      number       = {10},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2023-01128},
      pages        = {1387},
      year         = {2023},
      abstract     = {We have recently reported that in G2-phase cells (but not
                      S-phase cells) sustaining low loads of DNA double-strand
                      break (DSBs), ATM and ATR regulate the G2-checkpoint
                      epistatically, with ATR at the output-node, interfacing with
                      the cell cycle through Chk1. However, although inhibition of
                      ATR nearly completely abrogated the checkpoint, inhibition
                      of Chk1 using UCN-01 generated only partial responses. This
                      suggested that additional kinases downstream of ATR were
                      involved in the transmission of the signal to the cell cycle
                      engine. Additionally, the broad spectrum of kinases
                      inhibited by UCN-01 pointed to uncertainties in the
                      interpretation that warranted further investigations. Here,
                      we show that more specific Chk1 inhibitors exert an even
                      weaker effect on G2-checkpoint, as compared to ATR
                      inhibitors and UCN-01, and identify the MAPK p38α and its
                      downstream target MK2 as checkpoint effectors operating as
                      backup to Chk1. These observations further expand the
                      spectrum of p38/MK2 signaling to G2-checkpoint activation,
                      extend similar studies in cells exposed to other DNA
                      damaging agents and consolidate a role of p38/MK2 as a
                      backup kinase module, adding to similar backup functions
                      exerted in p53 deficient cells. The results extend the
                      spectrum of actionable strategies and targets in current
                      efforts to enhance the radiosensitivity in tumor cells.},
      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},
      doi          = {10.3390/cells12101387},
      url          = {https://inrepo02.dkfz.de/record/276747},
}