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@ARTICLE{Karbon:290533,
      author       = {G. Karbon and F. Schuler and V. Z. Braun and F. Eichin and
                      M. Haschka and M. Drach and R. Sotillo$^*$ and S. Geley and
                      D. C. Spierings and A. E. Tijhuis and F. Foijer and A.
                      Villunger},
      title        = {{C}hronic spindle assembly checkpoint activation causes
                      myelosuppression and gastrointestinal atrophy.},
      journal      = {EMBO reports},
      volume       = {25},
      number       = {6},
      issn         = {1469-221X},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2024-01150},
      pages        = {2743-2772},
      year         = {2024},
      note         = {2024 Jun;25(6):2743-2772},
      abstract     = {Interference with microtubule dynamics in mitosis activates
                      the spindle assembly checkpoint (SAC) to prevent chromosome
                      segregation errors. The SAC induces mitotic arrest by
                      inhibiting the anaphase-promoting complex (APC) via the
                      mitotic checkpoint complex (MCC). The MCC component MAD2
                      neutralizes the critical APC cofactor, CDC20, preventing
                      exit from mitosis. Extended mitotic arrest can promote
                      mitochondrial apoptosis and caspase activation. However, the
                      impact of mitotic cell death on tissue homeostasis in vivo
                      is ill-defined. By conditional MAD2 overexpression, we
                      observe that chronic SAC activation triggers bone marrow
                      aplasia and intestinal atrophy in mice. While
                      myelosuppression can be compensated for, gastrointestinal
                      atrophy is detrimental. Remarkably, deletion of
                      pro-apoptotic Bim/Bcl2l11 prevents gastrointestinal
                      syndrome, while neither loss of Noxa/Pmaip or co-deletion of
                      Bid and Puma/Bbc3 has such a protective effect, identifying
                      BIM as rate-limiting apoptosis effector in mitotic cell
                      death of the gastrointestinal epithelium. In contrast, only
                      overexpression of anti-apoptotic BCL2, but none of the
                      BH3-only protein deficiencies mentioned above, can mitigate
                      myelosuppression. Our findings highlight tissue and
                      cell-type-specific survival dependencies in response to SAC
                      perturbation in vivo.},
      keywords     = {Apoptosis (Other) / BH3-only Proteins (Other) / MAD2
                      (Other) / Mitosis (Other) / Spindle Assembly Checkpoint
                      (Other)},
      cin          = {B220},
      ddc          = {570},
      cid          = {I:(DE-He78)B220-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38806674},
      doi          = {10.1038/s44319-024-00160-3},
      url          = {https://inrepo02.dkfz.de/record/290533},
}