PXD018515 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | Pro-cognitive treatments restore hippocampal proteomic and kinome alterations in Ts65Dn mice |
Description | Down syndrome is the main genetic cause of intellectual disability and is due to triplication of human chromosome 21 (HSA21). Green tea extracts containing epigallocatechin-3-gallate (green tea) improve cognition both in mouse models and individuals with Down syndrome. We here analyzed the proteome and phosphoproteome alterations in a Down syndrome mouse model, the partial trisomic Ts65Dn mice, and the effect produced by the green tea extract and environmental enrichment (EE). Trisomic hippocampi presented a dysregulated proteome, especially when looking at the phosphorylation level in cognitive-related categories (synaptic proteins, neuronal projection, neuron development, microtubule), and GTPases/kinase activity and chromatin related categories. Green tea, EE, and their phospholipids in the plasma membrane and regulates signal transduction pathways, transcription factors, DNA methylation, mitochondrial function and phosphorylation, and autophagy to exert many of its beneficial biological actions Of interest for DS, it inhibits the activity of the Dual Specificity Tyrosine-Phosphorylation-Regulated Kinase 1A (DYRK1A), a DS candidate gene located in the 21q22.2 human chromosome region4,5. Previous work from our group showed that EGCG partially rescues the effects of overexpression of a DS candidate gene, DYRK1A, on the proteome and phosphoproteome of the hippocampus of TgDyrk1A mice6. However, the extent to which these mechanisms apply to a trisomy scenario is unknown. To get insight in these mechanisms we analyzed changes in protein abundances and phosphorylation in Ts65Dn mice, and their disomic counterparts in baseline conditions and upon three treatments known to improve cognition in Ts65Dn: i) green tea extract containing EGCG, ii) environmental enrichment (EE), and iii) their combination. |
HostingRepository | PRIDE |
AnnounceDate | 2024-10-22 |
AnnouncementXML | Submission_2024-10-22_05:13:27.523.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | Eduard Sabidó |
SpeciesList | scientific name: Mus musculus (Mouse); NCBI TaxID: 10090; |
ModificationList | phosphorylated residue; monohydroxylated residue; acetylated residue; iodoacetamide derivatized residue |
Instrument | LTQ Orbitrap Velos |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2020-04-14 01:53:22 | ID requested | |
1 | 2020-10-13 05:45:36 | announced | |
⏵ 2 | 2024-10-22 05:13:28 | announced | 2024-10-22: Updated project metadata. |
Publication List
De Toma I, Ortega M, Catuara-Solarz S, Sierra C, Sabid, ó E, Dierssen M, Re-establishment of the epigenetic state and rescue of kinome deregulation in Ts65Dn mice upon treatment with green tea extract and environmental enrichment. Sci Rep, 10(1):16023(2020) [pubmed] |
10.1038/s41598-020-72625-z; |
Keyword List
submitter keyword: hippocampus, phosphoproteome, Mouse,Ts65Dn, proteome |
Contact List
Eduard Sabido |
contact affiliation | Proteomics Unit, Center for Genomics Regulation, Universitat Pompeu Fabra, 08003 Barcelona, Spain |
contact email | eduard.sabido@crg.cat |
lab head | |
Eduard Sabidó |
contact affiliation | Centre de Regulació Genòmica |
contact email | eduard.sabido@crg.cat |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2020/10/PXD018515 |
PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD018515
- Label: PRIDE project
- Name: Pro-cognitive treatments restore hippocampal proteomic and kinome alterations in Ts65Dn mice