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@ARTICLE{Faletti:137579,
      author       = {L. Faletti and L. Peintner and S. Neumann and S. Sandler
                      and T. Grabinger and S. Mac Nelly and I. Merfort and C.-H.
                      Huang and D. F. Tschaharganeh$^*$ and T.-W. Kang$^*$ and F.
                      Heinzmann$^*$ and L. D'Artista$^*$ and U. Maurer and T.
                      Brunner and S. Lowe and L. Zender$^*$ and C. Borner},
      title        = {{TNF}α sensitizes hepatocytes to {F}as{L}-induced
                      apoptosis by {NF}κ{B}-mediated {F}as upregulation.},
      journal      = {Cell death $\&$ disease},
      volume       = {9},
      number       = {9},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2018-01459},
      pages        = {909},
      year         = {2018},
      abstract     = {Although it is well established that TNFα contributes to
                      hepatitis, liver failure and associated hepatocarcinogenesis
                      via the regulation of inflammation, its pro-apoptotic role
                      in the liver has remained enigmatic. On its own, TNFα is
                      unable to trigger apoptosis. However, when combined with the
                      transcriptional inhibitor GaLN, it can cause hepatocyte
                      apoptosis and liver failure in mice. Moreover, along with
                      others, we have shown that TNFα is capable of sensitizing
                      cells to FasL- or drug-induced cell death via c-Jun
                      N-terminal kinase (JNK) activation and
                      phosphorylation/activation of the BH3-only protein Bim. In
                      this context, TNFα could exacerbate hepatocyte cell death
                      during simultaneous inflammatory and T-cell-mediated immune
                      responses in the liver. Here we show that TNFα sensitizes
                      primary hepatocytes, established hepatocyte cell lines and
                      mouse embryo fibroblasts to FasL-induced apoptosis by the
                      transcriptional induction and higher surface expression of
                      Fas via the NFκB pathway. Genetic deletion, diminished
                      expression or dominant-negative inhibition of the NFκB
                      subunit p65 resulted in lower Fas expression and inhibited
                      TNFα-induced Fas upregulation and sensitization to
                      FasL-induced cell death. By hydrodynamic injection of p65
                      shRNA into the tail vein of mice, we confirm that Fas
                      upregulation by TNFα is also NFκB-mediated in the liver.
                      In conclusion, TNFα sensitization of FasL-induced apoptosis
                      in the liver proceeds via two parallel signaling pathways,
                      activation of JNK and Bim phosphorylation and NFκB-mediated
                      Fas upregulation.},
      cin          = {F190 / V076 / L801},
      ddc          = {570},
      cid          = {I:(DE-He78)F190-20160331 / I:(DE-He78)V076-20160331 /
                      I:(DE-He78)L801-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30185788},
      pmc          = {pmc:PMC6125596},
      doi          = {10.1038/s41419-018-0935-9},
      url          = {https://inrepo02.dkfz.de/record/137579},
}