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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},
}