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@ARTICLE{Mayr:285115,
      author       = {F. Mayr and V. Kruse and D. C. Fuhrmann and S. Wolf and J.
                      Löber and S. Alsouri and N. Paglilla and K. Lee and B.
                      Chapuy and B. Brüne and T. Zenz and B. Häupl$^*$ and T.
                      Oellerich$^*$ and M. Engelke},
      title        = {{SH}2 domain-containing inositol 5-phosphatases support the
                      survival of {B}urkitt lymphoma cells by promoting energy
                      metabolism.},
      journal      = {Haematologica},
      volume       = {109},
      number       = {5},
      issn         = {0390-6078},
      address      = {Pavia},
      publisher    = {Ferrata Storti Foundation},
      reportid     = {DKFZ-2023-02239},
      pages        = {1445-1459},
      year         = {2024},
      note         = {2024 May 1;109(5):1445-1459},
      abstract     = {Burkitt lymphoma cells (BL) exploit antigen-independent
                      tonic signals transduced by the B cell antigen receptor
                      (BCR) for their survival, but the molecular details of the
                      rewired BLspecific BCR signal network remain unclear. A loss
                      of function screen revealed the SH2 domain-containing
                      5`-inositol phosphatase 2 (SHIP2) as a potential modulator
                      of BL fitness. We characterized the role of SHIP2 in BL
                      survival in several BL cell models and show that perturbing
                      SHIP2 function renders cells more susceptible to apoptosis,
                      while attenuating proliferation in a BCR-dependent manner.
                      Unexpectedly, SHIP2 deficiency did neither affect PI3K
                      survival signals nor MAPK activity, but attenuated ATP
                      production. We found that an efficient energy metabolism in
                      BL cells requires phosphatidylinositol-3,4-bisphosphate
                      (PI(3,4)P2), which is the enzymatic product of SHIP
                      proteins. Consistently, interference with the function of
                      SHIP1 and SHIP2 augments BL cell susceptibility to PI3K
                      inhibition. Notably, we here provide a molecular basis of
                      how tonic BCR signals are connected to energy supply, which
                      is particularly important for such an aggressively growing
                      neoplasia. These findings may help to improve therapies for
                      the treatment of BL by limiting energy metabolism through
                      the inhibition of SHIP proteins, which renders BL cells more
                      susceptible to the targeting of survival signals.},
      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:37916396},
      doi          = {10.3324/haematol.2023.283663},
      url          = {https://inrepo02.dkfz.de/record/285115},
}