PXD009680 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | iTRAQ Protemics of mdx vs. mdx/Actg1-TG mouse skeletal muscle |
Description | Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by deleterious mutations in the DMD gene, rendering non-functional forms or complete absence of the protein dystrophin. Eccentric contraction-induced force loss is the most robust and reproducible phenotype of dystrophin-deficient skeletal muscle, yet the molecular mechanisms underlying force loss remain obscure. To this end, we utilized the mdx mouse model of DMD, which displays extreme sensitivity to eccentric contractions. An existing mouse line from our lab that overexpresses cytoplasmic gamma-actin specifically in skeletal muscle (mdx/Actg1-TG) was shown to significantly protect mdx muscle against contraction-induced force loss. To understand the mechanism behind this protection, we performed iTRAQ proteomics on mdx/Actg1-TG tibialis anterior (TA) muscle versus non-transgenic littermate controls to identify differentially-expressed proteins that may afford protection upon gamma-actin overexpression. |
HostingRepository | PRIDE |
AnnounceDate | 2020-11-10 |
AnnouncementXML | Submission_2020-11-10_06:10:26.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | James Ervasti |
SpeciesList | scientific name: Mus musculus (Mouse); NCBI TaxID: 10090; |
ModificationList | iTRAQ8plex-116 reporter+balance reagent acylated residue |
Instrument | LTQ Orbitrap Velos |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2018-05-04 07:37:06 | ID requested | |
1 | 2018-10-22 04:33:55 | announced | |
⏵ 2 | 2020-11-10 06:10:27 | announced | 2020-11-10: Updated publication reference for PubMed record(s): 30504831. |
Publication List
Olthoff JT, Lindsay A, Abo-Zahrah R, Baltgalvis KA, Patrinostro X, Belanto JJ, Yu DY, Perrin BJ, Garry DJ, Rodney GG, Lowe DA, Ervasti JM, Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle. Nat Commun, 9(1):5104(2018) [pubmed] |
Keyword List
curator keyword: Biomedical |
submitter keyword: Skeletal muscle, mdx, iTRAQ |
Contact List
James M. Ervasti |
contact affiliation | Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA |
contact email | jervasti@umn.edu |
lab head | |
James Ervasti |
contact affiliation | University of Minnesota |
contact email | ervastilab@gmail.com |
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/2018/10/PXD009680 |
PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD009680
- Label: PRIDE project
- Name: iTRAQ Protemics of mdx vs. mdx/Actg1-TG mouse skeletal muscle