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@ARTICLE{Chauhan:277799,
      author       = {C. Chauhan and A. Kraemer$^*$ and S. Knapp$^*$ and M.
                      Windheim and A. Kotlyarov and M. B. Menon and M. Gaestel},
      title        = {5-{I}odotubercidin sensitizes cells to {RIPK}1-dependent
                      necroptosis by interfering with {NF}κ{B} signaling.},
      journal      = {Cell death discovery},
      volume       = {9},
      number       = {1},
      issn         = {2058-7716},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2023-01510},
      pages        = {262},
      year         = {2023},
      abstract     = {Receptor-interacting protein kinases (RIPK)-1 and -3 play
                      crucial roles in cell fate decisions and are regulated by
                      multiple checkpoint controls. Previous studies have
                      identified IKK1/2- and p38/MK2-dependent checkpoints that
                      phosphorylate RIPK1 at different residues to inhibit its
                      activation. In this study, we investigated TNF-induced death
                      in MAPK-activated protein kinase 2 (MK2)-deficient cells and
                      found that MK2 deficiency or inactivation predominantly
                      leads to necroptotic cell death, even without caspase
                      inhibition. While RIPK1 inhibitors can rescue MK2-deficient
                      cells from necroptosis, inhibiting RIPK3 seems to switch the
                      process to apoptosis. To understand the underlying mechanism
                      of this switch, we screened a library of 149 kinase
                      inhibitors and identified the adenosine analog
                      5-Iodotubercidin (5-ITu) as the most potent compound that
                      sensitizes MK2-deficient MEFs to TNF-induced cell death.
                      5-ITu also enhances LPS-induced necroptosis when combined
                      with MK2 inhibition in RAW264.7 macrophages. Further
                      mechanistic studies revealed that 5-ITu induces
                      RIPK1-dependent necroptosis by suppressing IKK signaling in
                      the absence of MK2 activity. These findings highlight the
                      role for the multitarget kinase inhibitor 5-ITu in TNF-,
                      LPS- and chemotherapeutics-induced necroptosis and its
                      potential implications in RIPK1-targeted therapies.},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37495567},
      doi          = {10.1038/s41420-023-01576-x},
      url          = {https://inrepo02.dkfz.de/record/277799},
}