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@ARTICLE{Moreno:119959,
      author       = {N. Moreno and C. Schmidt$^*$ and J. Ahlfeld and J. Pöschl
                      and S. Dittmar and S. Pfister$^*$ and M. Kool$^*$ and K.
                      Kerl and U. Schüller},
      title        = {{L}oss of {S}marc proteins impairs cerebellar development.},
      journal      = {The journal of neuroscience},
      volume       = {34},
      number       = {40},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.44027},
      reportid     = {DKFZ-2017-00550},
      pages        = {13486-13491},
      year         = {2014},
      abstract     = {SMARCA4 (BRG1) and SMARCB1 (INI1) are tumor suppressor
                      genes that are crucially involved in the formation of
                      malignant rhabdoid tumors, such as atypical
                      teratoid/rhabdoid tumor (AT/RT). AT/RTs typically affect
                      infants and occur at various sites of the CNS with a
                      particular frequency in the cerebellum. Here, granule
                      neurons and their progenitors represent the most abundant
                      cell type and are known to give rise to a subset of
                      medulloblastoma, a histologically similar embryonal brain
                      tumor. To test how Smarc proteins influence the development
                      of granule neurons and whether this population may serve as
                      cellular origin for AT/RTs, we specifically deleted Smarca4
                      and Smarcb1 in cerebellar granule cell precursors.
                      Respective mutant mice displayed severe ataxia and motor
                      coordination deficits, but did not develop any tumors. In
                      fact, they suffered from a severely hypoplastic cerebellum
                      due to a significant inhibition of granule neuron precursor
                      proliferation. Molecularly, this was accompanied by an
                      enhanced activity of Wnt/β-catenin signaling that, by
                      itself, is known to cause a nearly identical phenotype. We
                      further used an hGFAP-cre allele, which deleted Smarcb1 much
                      earlier and in a wider neural precursor population, but we
                      still did not detect any tumor formation in the CNS. In
                      summary, our results emphasize cell-type-dependent roles of
                      Smarc proteins and argue against cerebellar granule cells
                      and other progeny of hGFAP-positive neural precursors as the
                      cellular origin for AT/RTs.},
      keywords     = {Atoh1 protein, mouse (NLM Chemicals) / Basic
                      Helix-Loop-Helix Transcription Factors (NLM Chemicals) /
                      Chromosomal Proteins, Non-Histone (NLM Chemicals) / Glial
                      Fibrillary Acidic Protein (NLM Chemicals) / Nuclear Proteins
                      (NLM Chemicals) / SMARCB1 Protein (NLM Chemicals) / Smarcb1
                      protein, mouse (NLM Chemicals) / Transcription Factors (NLM
                      Chemicals) / Wnt Proteins (NLM Chemicals) / Green
                      Fluorescent Proteins (NLM Chemicals) / Smarca4 protein,
                      mouse (NLM Chemicals) / DNA Helicases (NLM Chemicals) /
                      Phosphopyruvate Hydratase (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:25274825},
      doi          = {10.1523/JNEUROSCI.2560-14.2014},
      url          = {https://inrepo02.dkfz.de/record/119959},
}