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@ARTICLE{Talwar:275343,
      author       = {D. Talwar$^*$ and C. G. Miller$^*$ and J. Grossmann and L.
                      Szyrwiel and T. Schwecke and V. Demichev and A.-M. Mikecin
                      Drazic$^*$ and A. Mayakonda$^*$ and P. Lutsik$^*$ and C.
                      Veith$^*$ and M. Milsom$^*$ and K. Müller-Decker$^*$ and M.
                      Mülleder and M. Ralser and T. Dick$^*$},
      title        = {{T}he {GAPDH} redox switch safeguards reductive capacity
                      and enables survival of stressed tumour cells.},
      journal      = {Nature metabolism},
      volume       = {5},
      number       = {4},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2023-00712},
      pages        = {660-676},
      year         = {2023},
      note         = {DKFZ-ZMBH Alliance / 2023 Apr;5(4):660-676 /
                      #EA:A160#LA:A160#},
      abstract     = {Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is known
                      to contain an active-site cysteine residue undergoing
                      oxidation in response to hydrogen peroxide, leading to rapid
                      inactivation of the enzyme. Here we show that human and
                      mouse cells expressing a GAPDH mutant lacking this redox
                      switch retain catalytic activity but are unable to stimulate
                      the oxidative pentose phosphate pathway and enhance their
                      reductive capacity. Specifically, we find that
                      anchorage-independent growth of cells and spheroids is
                      limited by an elevation of endogenous peroxide levels and is
                      largely dependent on a functional GAPDH redox switch.
                      Likewise, tumour growth in vivo is limited by peroxide
                      stress and suppressed when the GAPDH redox switch is
                      disabled in tumour cells. The induction of additional
                      intratumoural oxidative stress by chemo- or radiotherapy
                      synergized with the deactivation of the GAPDH redox switch.
                      Mice lacking the GAPDH redox switch exhibit altered fatty
                      acid metabolism in kidney and heart, apparently in
                      compensation for the lack of the redox switch. Together, our
                      findings demonstrate the physiological and
                      pathophysiological relevance of oxidative GAPDH inactivation
                      in mammals.},
      cin          = {A160 / A012 / B370 / W420},
      ddc          = {610},
      cid          = {I:(DE-He78)A160-20160331 / I:(DE-He78)A012-20160331 /
                      I:(DE-He78)B370-20160331 / I:(DE-He78)W420-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37024754},
      doi          = {10.1038/s42255-023-00781-3},
      url          = {https://inrepo02.dkfz.de/record/275343},
}