Loss of full-length dystrophin expression results in major cell-autonomous abnormalities in proliferating myoblasts.
DMD
dystrophin
human
mdx
medicine
mouse
myoblast
transcriptomics
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
27 09 2022
27 09 2022
Historique:
received:
12
11
2021
accepted:
02
09
2022
entrez:
27
9
2022
pubmed:
28
9
2022
medline:
30
9
2022
Statut:
epublish
Résumé
Duchenne muscular dystrophy (DMD) affects myofibers and muscle stem cells, causing progressive muscle degeneration and repair defects. It was unknown whether dystrophic myoblasts-the effector cells of muscle growth and regeneration-are affected. Using transcriptomic, genome-scale metabolic modelling and functional analyses, we demonstrate, for the first time, convergent abnormalities in primary mouse and human dystrophic myoblasts. In
Identifiants
pubmed: 36164827
doi: 10.7554/eLife.75521
pii: 75521
pmc: PMC9514850
doi:
pii:
Substances chimiques
Dystrophin
0
Fatty Acids
0
Leukotrienes
0
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2022, Gosselin et al.
Déclaration de conflit d'intérêts
MG, VM, MB, SV, AO, JR, LB, MK, CA, CP, DG No competing interests declared, SR SR received royalties from Cancer Research Technology Ltd through University of Cambridge Enterprise Ltd under agreement A13086 for "Chromatin-bound METTL3 m6A methyltransferase facilitates myeloid leukaemogenesis by modulating ribosome stalling"
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