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@ARTICLE{Feng:128622,
      author       = {W. Feng$^*$ and C. Shao$^*$ and H.-K. Liu$^*$},
      title        = {{V}ersatile {R}oles of the {C}hromatin {R}emodeler {CHD}7
                      during {B}rain {D}evelopment and {D}isease.},
      journal      = {Frontiers in molecular neuroscience},
      volume       = {10},
      issn         = {1662-5099},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DKFZ-2017-04638},
      pages        = {309},
      year         = {2017},
      note         = {DKFZ-ZMBH-Allianz},
      abstract     = {CHD7 (Chromo-Helicase-DNA binding protein 7) protein is an
                      ATP-dependent chromatin remodeler. Heterozygous mutation of
                      the CHD7 gene causes a severe congenital disease known as
                      CHARGE syndrome. Most CHARGE syndrome patients have brain
                      structural anomalies, implicating an important role of CHD7
                      during brain development. In this review, we summarize
                      studies dissecting developmental functions of CHD7 in the
                      brain and discuss pathogenic mechanisms behind
                      neurodevelopmental defects caused by mutation of CHD7. As we
                      discussed, CHD7 protein exhibits a remarkably specific and
                      dynamic expression pattern in the brain. Studies in human
                      and animal models have revealed that CHD7 is involved in
                      multiple developmental lineages and processes in the brain.
                      Mechanistically, CHD7 is essential for neural
                      differentiation due to its transcriptional regulation in
                      progenitor cells.},
      subtyp        = {Review Article},
      cin          = {A240},
      ddc          = {610},
      cid          = {I:(DE-He78)A240-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29033785},
      pmc          = {pmc:PMC5625114},
      doi          = {10.3389/fnmol.2017.00309},
      url          = {https://inrepo02.dkfz.de/record/128622},
}