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@ARTICLE{He:120198,
      author       = {X. He and L. Zhang and Y. Chen and M. Remke and D. Shih and
                      F. Lu and H. Wang and Y. Deng and Y. Yu and Y. Xia and X. Wu
                      and V. Ramaswamy and T. Hu and F. Wang and W. Zhou and D. K.
                      Burns and S. H. Kim and M. Kool$^*$ and S. Pfister$^*$ and
                      L. S. Weinstein and S. L. Pomeroy and R. J. Gilbertson and
                      J. B. Rubin and Y. Hou and R. Wechsler-Reya and M. D. Taylor
                      and Q. R. Lu},
      title        = {{T}he {G} protein α subunit {G}αs is a tumor suppressor
                      in {S}onic hedgehog-driven medulloblastoma.},
      journal      = {Nature medicine},
      volume       = {20},
      number       = {9},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2017-00780},
      pages        = {1035 - 1042},
      year         = {2014},
      abstract     = {Medulloblastoma, the most common malignant childhood brain
                      tumor, exhibits distinct molecular subtypes and cellular
                      origins. Genetic alterations driving medulloblastoma
                      initiation and progression remain poorly understood. Herein,
                      we identify GNAS, encoding the G protein Gαs, as a potent
                      tumor suppressor gene that, when expressed at low levels,
                      defines a subset of aggressive Sonic hedgehog (SHH)-driven
                      human medulloblastomas. Ablation of the single Gnas gene in
                      anatomically distinct progenitors in mice is sufficient to
                      induce Shh-associated medulloblastomas, which recapitulate
                      their human counterparts. Gαs is highly enriched at the
                      primary cilium of granule neuron precursors and suppresses
                      Shh signaling by regulating both the cAMP-dependent pathway
                      and ciliary trafficking of Hedgehog pathway components.
                      Elevation in levels of a Gαs effector, cAMP, effectively
                      inhibits tumor cell proliferation and progression in
                      Gnas-ablated mice. Thus, our gain- and loss-of-function
                      studies identify a previously unrecognized tumor suppressor
                      function for Gαs that can be found consistently across
                      Shh-group medulloblastomas of disparate cellular and
                      anatomical origins, highlighting G protein modulation as a
                      potential therapeutic avenue.},
      keywords     = {Hedgehog Proteins (NLM Chemicals) / Cyclic AMP (NLM
                      Chemicals) / GTP-Binding Protein alpha Subunits, Gs (NLM
                      Chemicals)},
      cin          = {B062},
      ddc          = {610},
      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:25150496},
      pmc          = {pmc:PMC4334261},
      doi          = {10.1038/nm.3666},
      url          = {https://inrepo02.dkfz.de/record/120198},
}