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000162815 0247_ $$2doi$$a10.1073/pnas.2009393118
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000162815 037__ $$aDZNE-2021-01470
000162815 041__ $$aEnglish
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000162815 1001_ $$0P:(DE-2719)2810985$$aSchlusche, Anna Katharina$$b0$$eFirst author$$udzne
000162815 245__ $$aDevelopmental HCN channelopathy results in decreased neural progenitor proliferation and microcephaly in mice.
000162815 260__ $$aWashington, DC$$bNational Acad. of Sciences$$c2021
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000162815 520__ $$aThe 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.
000162815 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
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000162815 650_7 $$2Other$$aHCN channelopathy
000162815 650_7 $$2Other$$abrain development
000162815 650_7 $$2Other$$acell cycle
000162815 650_7 $$2Other$$amicrocephaly
000162815 650_2 $$2MeSH$$aAnimals
000162815 650_2 $$2MeSH$$aCell Cycle
000162815 650_2 $$2MeSH$$aCell Death
000162815 650_2 $$2MeSH$$aCell Proliferation: physiology
000162815 650_2 $$2MeSH$$aCells, Cultured
000162815 650_2 $$2MeSH$$aCerebral Cortex: cytology
000162815 650_2 $$2MeSH$$aCerebral Cortex: embryology
000162815 650_2 $$2MeSH$$aChannelopathies: embryology
000162815 650_2 $$2MeSH$$aChannelopathies: etiology
000162815 650_2 $$2MeSH$$aEmbryonic Stem Cells: metabolism
000162815 650_2 $$2MeSH$$aEmbryonic Stem Cells: physiology
000162815 650_2 $$2MeSH$$aHumans
000162815 650_2 $$2MeSH$$aHyperpolarization-Activated Cyclic Nucleotide-Gated Channels: antagonists & inhibitors
000162815 650_2 $$2MeSH$$aHyperpolarization-Activated Cyclic Nucleotide-Gated Channels: genetics
000162815 650_2 $$2MeSH$$aHyperpolarization-Activated Cyclic Nucleotide-Gated Channels: metabolism
000162815 650_2 $$2MeSH$$aHyperpolarization-Activated Cyclic Nucleotide-Gated Channels: physiology
000162815 650_2 $$2MeSH$$aMice
000162815 650_2 $$2MeSH$$aMice, Transgenic
000162815 650_2 $$2MeSH$$aMicrocephaly: embryology
000162815 650_2 $$2MeSH$$aMicrocephaly: etiology
000162815 650_2 $$2MeSH$$aNeural Stem Cells: metabolism
000162815 650_2 $$2MeSH$$aNeural Stem Cells: physiology
000162815 650_2 $$2MeSH$$aNeurogenesis: physiology
000162815 650_2 $$2MeSH$$aRats
000162815 7001_ $$00000-0002-3289-7807$$aVay, Sabine Ulrike$$b1
000162815 7001_ $$aKleinenkuhnen, Niklas$$b2
000162815 7001_ $$aSandke, Steffi$$b3
000162815 7001_ $$aCampos-Martín, Rafael$$b4
000162815 7001_ $$00000-0002-6168-005X$$aFlorio, Marta$$b5
000162815 7001_ $$00000-0003-4143-7201$$aHuttner, Wieland$$b6
000162815 7001_ $$00000-0002-4146-6371$$aTresch, Achim$$b7
000162815 7001_ $$aRoeper, Jochen$$b8
000162815 7001_ $$00000-0001-8036-395X$$aRueger, Maria Adele$$b9
000162815 7001_ $$0P:(DE-2719)2811046$$aJakovcevski, Igor$$b10$$udzne
000162815 7001_ $$0P:(DE-2719)2810965$$aStockebrand, Malte$$b11$$udzne
000162815 7001_ $$0P:(DE-2719)2810976$$aIsbrandt, Dirk$$b12$$eLast author$$udzne
000162815 773__ $$0PERI:(DE-600)1461794-8$$a10.1073/pnas.2009393118$$gVol. 118, no. 35, p. e2009393118 -$$n35$$pe2009393118$$tProceedings of the National Academy of Sciences of the United States of America$$v118$$x1091-6490$$y2021
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