ArticleStem cells (Dayton, Ohio)2024
Dual-specificity phosphatases 13 and 27 as key switches in muscle stem cell transition from proliferation to differentiation.
Article in Stem cells (Dayton, Ohio), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Identification of a Diagnostic Gene Signature Associated with Centrosome Amplification in Pressure Injuries: A Cross-Sectional Transcriptome and Machine Learning Study.Journal of inflammation research · 2026Article
- Large MAF transcription factors reawaken evolutionarily dormant fast-glycolytic type IIb myofibers in human skeletal muscle.Skeletal muscle · 2025Article
- Integrating Physical and Biochemical Cues for Muscle Engineering: Scaffolds and Graft Durability.Bioengineering (Basel, Switzerland) · 2024Review
- Effect of spermidine intake on skeletal muscle regeneration after chemical injury in male mice.Physiological reports · 2024Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Muscle regeneration depends on muscle stem cell (MuSC) activity. Myogenic regulatory factors, including myoblast determination protein 1 (MyoD), regulate the fate transition of MuSCs. However, the direct target of MYOD in the process is not completely clear. Using previously established MyoD knock-in (MyoD-KI) mice, we revealed that MyoD targets dual-specificity phosphatase (Dusp) 13 and Dusp27. In Dusp13:Dusp27 double knock-out mice, the ability for muscle regeneration after injury was reduced. Moreover, single-cell RNA sequencing of MyoD-high expressing MuSCs from MyoD-KI mice revealed that Dusp13 and Dusp27 are expressed only in specific populations within MyoD-high MuSCs, which also express Myogenin. Overexpressing Dusp13 in MuSCs causes premature muscle differentiation. Thus, we propose a model where DUSP13 and DUSP27 contribute to the fate transition of MuSCs from proliferation to differentiation during myogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.