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@ARTICLE{Wu:131629,
      author       = {X. Wu and L.-S. Zhang and J. Toombs and Y.-C. Kuo and J. T.
                      Piazza and R. Tuladhar and Q. Barrett and C.-W. Fan and X.
                      Zhang and L. D. Walensky and M. Kool$^*$ and S. Y. Cheng and
                      R. Brekken and J. T. Opferman and D. R. Green and T.
                      Moldoveanu and L. Lum},
      title        = {{E}xtra-mitochondrial prosurvival {BCL}-2 proteins regulate
                      gene transcription by inhibiting the {SUFU} tumour
                      suppressor.},
      journal      = {Nature cell biology},
      volume       = {19},
      number       = {10},
      issn         = {1476-4679},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DKFZ-2017-06261},
      pages        = {1226 - 1236},
      year         = {2017},
      abstract     = {Direct interactions between pro- and anti-apoptotic BCL-2
                      family members form the basis of cell death decision-making
                      at the outer mitochondrial membrane (OMM). Here we report
                      that three anti-apoptotic BCL-2 proteins (MCL-1, BCL-2 and
                      BCL-XL) found untethered from the OMM function as
                      transcriptional regulators of a prosurvival and growth
                      program. Anti-apoptotic BCL-2 proteins engage a BCL-2
                      homology (BH) domain sequence found in SUFU (suppressor of
                      fused), a tumour suppressor and antagonist of the GLI
                      DNA-binding proteins. BCL-2 proteins directly promote SUFU
                      turnover, inhibit SUFU-GLI interaction, and induce the
                      expression of the GLI target genes BCL-2, MCL-1 and BCL-XL.
                      Anti-apoptotic BCL-2 protein/SUFU feedforward signalling
                      promotes cancer cell survival and growth, and can be
                      disabled with BH3 mimetics-small molecules that target
                      anti-apoptotic BCL-2 proteins. Our findings delineate a
                      chemical strategy for countering drug resistance in
                      GLI-associated tumours and reveal unanticipated functions
                      for BCL-2 proteins as transcriptional regulators.},
      keywords     = {Antineoplastic Agents (NLM Chemicals) / BCL2 protein, human
                      (NLM Chemicals) / BCL2L1 protein, human (NLM Chemicals) /
                      Bax protein (53-86) (NLM Chemicals) / Bcl2l1 protein, mouse
                      (NLM Chemicals) / GLI1 protein, human (NLM Chemicals) / Gli
                      protein, mouse (NLM Chemicals) / MCL1 protein, human (NLM
                      Chemicals) / Mcl1 protein, mouse (NLM Chemicals) / Myeloid
                      Cell Leukemia Sequence 1 Protein (NLM Chemicals) / Peptide
                      Fragments (NLM Chemicals) / Proto-Oncogene Proteins (NLM
                      Chemicals) / Proto-Oncogene Proteins c-bcl-2 (NLM Chemicals)
                      / Repressor Proteins (NLM Chemicals) / SUFU protein, human
                      (NLM Chemicals) / Sufu protein, mouse (NLM Chemicals) /
                      Tumor Suppressor Proteins (NLM Chemicals) / Zinc Finger
                      Protein GLI1 (NLM Chemicals) / bcl-X Protein (NLM Chemicals)
                      / Bcl2 protein, mouse (NLM Chemicals)},
      cin          = {B062},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28945232},
      pmc          = {pmc:PMC5657599},
      doi          = {10.1038/ncb3616},
      url          = {https://inrepo02.dkfz.de/record/131629},
}