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@ARTICLE{Gdynia:125881,
      author       = {G. P. Gdynia$^*$ and S. W. Sauer and J. Kopitz$^*$ and D.
                      Fuchs and K. Duglova and T. Ruppert and M. Miller$^*$ and J.
                      Pahl$^*$ and A. Cerwenka$^*$ and M. Enders and H. Mairbäurl
                      and M. M. Kamiński$^*$ and R. Penzel and C. Zhang and J. C.
                      Fuller and R. C. Wade and A. Benner$^*$ and J. Chang$^*$ and
                      H. Brenner$^*$ and M. Hoffmeister$^*$ and H. Zentgraf$^*$
                      and P. Schirmacher and W. Roth$^*$},
      title        = {{T}he {HMGB}1 protein induces a metabolic type of tumour
                      cell death by blocking aerobic respiration.},
      journal      = {Nature Communications},
      volume       = {7},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-02005},
      pages        = {10764 -},
      year         = {2016},
      abstract     = {The high-mobility group box 1 (HMGB1) protein has a central
                      role in immunological antitumour defense. Here we show that
                      natural killer cell-derived HMGB1 directly eliminates cancer
                      cells by triggering metabolic cell death. HMGB1
                      allosterically inhibits the tetrameric pyruvate kinase
                      isoform M2, thus blocking glucose-driven aerobic
                      respiration. This results in a rapid metabolic shift forcing
                      cells to rely solely on glycolysis for the maintenance of
                      energy production. Cancer cells can acquire resistance to
                      HMGB1 by increasing glycolysis using the dimeric form of
                      PKM2, and employing glutaminolysis. Consistently, we observe
                      an increase in the expression of a key enzyme of
                      glutaminolysis, malic enzyme 1, in advanced colon cancer.
                      Moreover, pharmaceutical inhibition of glutaminolysis
                      sensitizes tumour cells to HMGB1 providing a basis for a
                      therapeutic strategy for treating cancer.},
      keywords     = {Carrier Proteins (NLM Chemicals) / HMGB1 Protein (NLM
                      Chemicals) / Membrane Proteins (NLM Chemicals) / Thyroid
                      Hormones (NLM Chemicals) / thyroid hormone-binding proteins
                      (NLM Chemicals) / Glucose (NLM Chemicals)},
      cin          = {C060 / C020 / C070 / D080 / G110 / G105 / G150},
      ddc          = {500},
      cid          = {I:(DE-He78)C060-20160331 / I:(DE-He78)C020-20160331 /
                      I:(DE-He78)C070-20160331 / I:(DE-He78)D080-20160331 /
                      I:(DE-He78)G110-20160331 / I:(DE-He78)G105-20160331 /
                      I:(DE-He78)G150-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26948869},
      pmc          = {pmc:PMC4786644},
      doi          = {10.1038/ncomms10764},
      url          = {https://inrepo02.dkfz.de/record/125881},
}