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Cell cycle and cell size regulation in Down Syndrome cells | SpringerLink
Description:
Although the neuropathological features typical for Down Syndrome obviously result from deregulation of both, cell cycle control and differentiation processes, so far research focused on the latter. Considering the known similarities between the neuropathology of...
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g1-cyclin-dependent kinases privacy choices/manage cookies cyclin-dependent kinases download preview pdf editor information editors mammalian cell cycle s100 protein family amniotic fluid cells cell cycle phases ongoing cell cycle european economic area neuropathological features typical significant differences suggesting dyrk1a regulate axonal e2f-1-induced apoptosis human cell lines population-based study normal animal proliferation conditions privacy policy cell cycle control journal finder publish cell size regulation accepting optional cookies book series advanced maternal age cell cycle activation main content log disease neuronal degeneration c-myc chapter cite cell proliferation syndrome research cell cycle research focused privacy policy check access ethics access personal data cell size permissions reprints neural suppl journal publish lubec rights trisomy 21 cells chapter advances optional cookies syndrome cells manage preferences human chromosome 21 cell biology
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ScholarlyArticle:
headline:Cell cycle and cell size regulation in Down Syndrome cells
pageEnd:58
pageStart:51
image:https://media.springernature.com/w153/springer-static/cover/book/978-3-7091-6721-2.jpg
genre:
Medicine
Medicine (R0)
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name:Advances in Down Syndrome Research
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978-3-7091-6721-2
978-3-211-40776-9
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name:Springer Vienna
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author:
name:M. Rosner
affiliation:
name:University of Vienna
address:
name:Obstetrics and Gynecology, Prenatal Diagnosis and Therapy, University of Vienna, Vienna, Austria
type:PostalAddress
type:Organization
type:Person
name:A. Kowalska
affiliation:
name:University of Vienna
address:
name:Obstetrics and Gynecology, Prenatal Diagnosis and Therapy, University of Vienna, Vienna, Austria
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name:A. Freilinger
affiliation:
name:University of Vienna
address:
name:Obstetrics and Gynecology, Prenatal Diagnosis and Therapy, University of Vienna, Vienna, Austria
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name:A-R. Prusa
affiliation:
name:University of Vienna
address:
name:Obstetrics and Gynecology, Prenatal Diagnosis and Therapy, University of Vienna, Vienna, Austria
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name:E. Marton
affiliation:
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address:
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name:M. Hengstschläger
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keywords:Down Syndrome, Cell Cycle Control, Cell Cycle Phase, Additional Chromosome, Cell Cycle Activation
description:Although the neuropathological features typical for Down Syndrome obviously result from deregulation of both, cell cycle control and differentiation processes, so far research focused on the latter. Considering the known similarities between the neuropathology of Down Syndrome and Alzheimer’s disease and the knowledge, that in Alzheimer’s disease neuronal degeneration is associated with the activation of mitogenic signals and cell cycle activation, it is tempting to investigate the consequences of an additional chromosome 21 on mammalian cell cycle regulation. We analysed the distribution of cells in different cell cycle phases on the flowcytometer and the cell size of human amniotic fluid cells with normal karyotypes and with trisomy 21. We could not detect any significant differences suggesting that the presence of an additional copy of the about 225 genes on human chromosome 21 does not trigger cell cycle effects in amniotic fluid cells. These data provide new insights into the cell biology of trisomy 21 cells.
datePublished:2003
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