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@ARTICLE{Schlusche:162815,
      author       = {Schlusche, Anna Katharina and Vay, Sabine Ulrike and
                      Kleinenkuhnen, Niklas and Sandke, Steffi and Campos-Martín,
                      Rafael and Florio, Marta and Huttner, Wieland and Tresch,
                      Achim and Roeper, Jochen and Rueger, Maria Adele and
                      Jakovcevski, Igor and Stockebrand, Malte and Isbrandt, Dirk},
      title        = {{D}evelopmental {HCN} channelopathy results in decreased
                      neural progenitor proliferation and microcephaly in mice.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {118},
      number       = {35},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DZNE-2021-01470},
      pages        = {e2009393118},
      year         = {2021},
      abstract     = {The development of the cerebral cortex relies on the
                      controlled division of neural stem and progenitor cells. The
                      requirement for precise spatiotemporal control of
                      proliferation and cell fate places a high demand on the cell
                      division machinery, and defective cell division can cause
                      microcephaly and other brain malformations. Cell-extrinsic
                      and -intrinsic factors govern the capacity of cortical
                      progenitors to produce large numbers of neurons and glia
                      within a short developmental time window. In particular, ion
                      channels shape the intrinsic biophysical properties of
                      precursor cells and neurons and control their membrane
                      potential throughout the cell cycle. We found that
                      hyperpolarization-activated cyclic nucleotide-gated cation
                      (HCN) channel subunits are expressed in mouse, rat, and
                      human neural progenitors. Loss of HCN channel function in
                      rat neural stem cells impaired their proliferation by
                      affecting the cell-cycle progression, causing G1
                      accumulation and dysregulation of genes associated with
                      human microcephaly. Transgene-mediated, dominant-negative
                      loss of HCN channel function in the embryonic mouse
                      telencephalon resulted in pronounced microcephaly. Together,
                      our findings suggest a role for HCN channel subunits as a
                      part of a general mechanism influencing cortical development
                      in mammals.},
      keywords     = {Animals / Cell Cycle / Cell Death / Cell Proliferation:
                      physiology / Cells, Cultured / Cerebral Cortex: cytology /
                      Cerebral Cortex: embryology / Channelopathies: embryology /
                      Channelopathies: etiology / Embryonic Stem Cells: metabolism
                      / Embryonic Stem Cells: physiology / Humans /
                      Hyperpolarization-Activated Cyclic Nucleotide-Gated
                      Channels: antagonists $\&$ inhibitors /
                      Hyperpolarization-Activated Cyclic Nucleotide-Gated
                      Channels: genetics / Hyperpolarization-Activated Cyclic
                      Nucleotide-Gated Channels: metabolism /
                      Hyperpolarization-Activated Cyclic Nucleotide-Gated
                      Channels: physiology / Mice / Mice, Transgenic /
                      Microcephaly: embryology / Microcephaly: etiology / Neural
                      Stem Cells: metabolism / Neural Stem Cells: physiology /
                      Neurogenesis: physiology / Rats / HCN channelopathy (Other)
                      / brain development (Other) / cell cycle (Other) /
                      microcephaly (Other)},
      cin          = {AG Isbrandt},
      ddc          = {500},
      cid          = {I:(DE-2719)1011003},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34429357},
      pmc          = {pmc:PMC8536352},
      doi          = {10.1073/pnas.2009393118},
      url          = {https://pub.dzne.de/record/162815},
}