Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS
dc.contributor.author
Abd Alla, Joshua
dc.contributor.author
Quitterer, Ursula
dc.contributor.author
Abd Alla
dc.date.accessioned
2024-04-30T11:56:17Z
dc.date.available
2022-01-21T17:47:36Z
dc.date.available
2022-04-13T10:47:29Z
dc.date.available
2022-04-14T10:52:11Z
dc.date.available
2024-04-30T11:56:17Z
dc.date.issued
2021-12-27
dc.identifier.uri
http://hdl.handle.net/20.500.11850/527568
dc.description.abstract
The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. In addition, the study determined the cardiac transcriptomes of GRK2-transgenic mice. Tg-GRK2 mice have a slightly increased transgenic expression of GRK2. According to NGS data, cardiac GRK2-Grk2 transcript levels of Tg-GRK2 mice are 1.59±0.10-fold higher than those of non-transgenic FVB hearts. In Tg-GRK2 mice, transgenic GRK2 is expressed under control of the ubiquitous CMV immediate-early promoter/enhancer. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic RKIP expression and cardiac degeneration induced by GRK2 expression.
en_US
dc.language.iso
en
en_US
dc.publisher
NCBI GEO database
en_US
dc.subject
NGS
en_US
dc.title
Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS
en_US
dc.type
Dataset
ethz.publication.place
Bethesda
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03735 - Quitterer, Ursula M. / Quitterer, Ursula M.
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03735 - Quitterer, Ursula M. / Quitterer, Ursula M.
en_US
ethz.identifier.url
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE191316
ethz.relation.isSupplementTo
10.3929/ethz-b-000533339
ethz.date.deposited
2022-01-21T17:47:55Z
ethz.source
FORM
ethz.eth
yes
en_US
ethz.availability
Metadata only
en_US
ethz.rosetta.installDate
2022-04-13T10:48:10Z
ethz.rosetta.lastUpdated
2023-02-07T00:48:58Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.repository
Gene Expression Omnibus
en_US
ethz.COinS
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