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@ARTICLE{Kyrkou:291067,
      author       = {A. Kyrkou$^*$ and R. Valla$^*$ and Y. Zhang$^*$ and G.
                      Ambrosi$^*$ and S. Laier$^*$ and K. Müller-Decker$^*$ and
                      M. Boutros$^*$ and A. Teleman$^*$},
      title        = {{G}6{PD} and {ACSL}3 are synthetic lethal partners of {NF}2
                      in {S}chwann cells.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2024-01287},
      pages        = {5115},
      year         = {2024},
      note         = {#EA:B140#LA:B140#},
      abstract     = {Neurofibromatosis Type II (NFII) is a genetic condition
                      caused by loss of the NF2 gene, resulting in activation of
                      the YAP/TAZ pathway and recurrent Schwann cell tumors, as
                      well as meningiomas and ependymomas. Unfortunately, few
                      pharmacological options are available for NFII. Here, we
                      undertake a genome-wide CRISPR/Cas9 screen to search for
                      synthetic-lethal genes that, when inhibited, cause death of
                      NF2 mutant Schwann cells but not NF2 wildtype cells. We
                      identify ACSL3 and G6PD as two synthetic-lethal partners for
                      NF2, both involved in lipid biogenesis and cellular redox.
                      We find that NF2 mutant Schwann cells are more oxidized than
                      control cells, in part due to reduced expression of genes
                      involved in NADPH generation such as ME1. Since G6PD and ME1
                      redundantly generate cytosolic NADPH, lack of either one is
                      compatible with cell viability, but not down-regulation of
                      both. Since genetic deficiency for G6PD is tolerated in the
                      human population, G6PD could be a good pharmacological
                      target for NFII.},
      keywords     = {Schwann Cells: metabolism / Humans / CRISPR-Cas Systems /
                      Glucosephosphate Dehydrogenase: metabolism /
                      Glucosephosphate Dehydrogenase: genetics / Neurofibromin 2:
                      metabolism / Neurofibromin 2: genetics / Coenzyme A Ligases:
                      metabolism / Coenzyme A Ligases: genetics / Synthetic Lethal
                      Mutations / Animals / Neurofibromatosis 2: metabolism /
                      Neurofibromatosis 2: genetics / NADP: metabolism / Mice /
                      Oxidation-Reduction / Glucosephosphate Dehydrogenase (NLM
                      Chemicals) / Neurofibromin 2 (NLM Chemicals) / Coenzyme A
                      Ligases (NLM Chemicals) / long-chain-fatty-acid-CoA ligase
                      (NLM Chemicals) / G6PD protein, human (NLM Chemicals) / NADP
                      (NLM Chemicals) / NF2 protein, human (NLM Chemicals)},
      cin          = {B140 / B110 / W420},
      ddc          = {500},
      cid          = {I:(DE-He78)B140-20160331 / I:(DE-He78)B110-20160331 /
                      I:(DE-He78)W420-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38879607},
      pmc          = {pmc:PMC11180199},
      doi          = {10.1038/s41467-024-49298-7},
      url          = {https://inrepo02.dkfz.de/record/291067},
}