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dc.contributor.author
Cramer, Nathan P.
dc.contributor.author
Best, Tyler K.
dc.contributor.author
Stoffel, Marcus
dc.contributor.author
Siarey, Richard J.
dc.contributor.author
Galdzicki, Zygmunt
dc.contributor.editor
Blackburn, Thomas P.
dc.date.accessioned
2023-10-20T12:54:45Z
dc.date.available
2017-06-09T09:04:40Z
dc.date.available
2023-10-20T12:54:45Z
dc.date.issued
2010
dc.identifier.isbn
978-0-12-378647-0
en_US
dc.identifier.issn
1054-3589
dc.identifier.issn
1557-8925
dc.identifier.other
10.1016/S1054-3589(10)58015-3
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/29306
dc.description.abstract
Down syndrome (DS) results from the presence of an extra copy of genes on the long-arm of chromosome 21. Aberrant expression of these trisomic genes leads to widespread neurological changes that vary in their severity. However, how the presence of extra genes affects the physiological and behavioral phenotypes associated with DS is not well understood. The most likely cause of the complex DS phenotypes is the overexpression of dosage-sensitive genes. However, other factors, such as the complex interactions between gene products as proteins and noncoding RNAs, certainly play significant roles contributing to the spectrum of severity. Here we will review evidence regarding how the overexpression of one particular gene encoding for G-protein-activated inward rectifying potassium type 2 (GIRK2) channel subunit and its coupling to GABAB receptors may contribute to a range of mental and functional disabilities in DS.
en_US
dc.language.iso
en
en_US
dc.publisher
Academic Press
en_US
dc.subject
GIRK2 Knockout Trisomy 21
en_US
dc.subject
gene dosage
en_US
dc.subject
mental retardation
en_US
dc.subject
hippocampus
en_US
dc.subject
long-term potentiation
en_US
dc.subject
Ts65Dn
en_US
dc.title
GABAB–GIRK2-Mediated Signaling in Down Syndrome
en_US
dc.type
Book Chapter
dc.date.published
2010-07-22
ethz.book.title
GABABReceptor Pharmacology: A Tribute to Norman Bowery
en_US
ethz.journal.title
Advances in Pharmacology
ethz.journal.volume
58
en_US
ethz.pages.start
397
en_US
ethz.pages.end
426
en_US
ethz.publication.place
New York, NY
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03739 - Stoffel, Markus / Stoffel, Markus
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03739 - Stoffel, Markus / Stoffel, Markus
ethz.date.deposited
2017-06-09T09:04:46Z
ethz.source
ECIT
ethz.identifier.importid
imp59364d98091bd43257
ethz.ecitpid
pub:48719
ethz.eth
yes
en_US
ethz.availability
Metadata only
en_US
ethz.rosetta.installDate
2017-07-14T23:48:29Z
ethz.rosetta.lastUpdated
2024-02-03T05:27:40Z
ethz.rosetta.versionExported
true
ethz.COinS
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