ArticleCell cycle (Georgetown, Tex.)2011
Coordination of cell cycle, DNA repair and muscle gene expression in myoblasts exposed to genotoxic stress.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- RNF138 regulates skeletal muscle differentiation via the Wnt/β-catenin signaling pathway.Theranostics · 2025Article
- DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation.Genes & development · 2017Article
- The Spindle Assembly Checkpoint Safeguards Genomic Integrity of Skeletal Muscle Satellite Cells.Stem cell reports · 2015Article
- Muscle gets stressed? p53 represses and protects.Cell death and differentiation · 2015Article
- DNA damage-activated ABL-MyoD signaling contributes to DNA repair in skeletal myoblasts.Cell death and differentiation · 2013Article
- The mysterious human epidermal cell cycle, or an oncogene-induced differentiation checkpoint.Cell cycle (Georgetown, Tex.) · 2012Review
- Checking before changing: cell cycle checkpoints inhibit muscle differentiation.Cell cycle (Georgetown, Tex.) · 2011Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Upon exposure to genotoxic stress, skeletal muscle progenitors coordinate DNA repair and the activation of the differentiation program through the DNA damage-activated differentiation checkpoint, which holds the transcription of differentiation genes while the DNA is repaired. A conceptual hurdle intrinsic to this process relates to the coordination of DNA repair and muscle-specific gene transcription within specific cell cycle boundaries (cell cycle checkpoints) activated by different types of genotoxins. Here, we show that, in proliferating myoblasts, the inhibition of muscle gene transcription occurs by either a G 1- or G 2-specific differentiation checkpoint. In response to genotoxins that induce G 1 arrest, MyoD binds target genes but is functionally inactivated by a c-Abl-dependent phosphorylation. In contrast, DNA damage-activated G 2 checkpoint relies on the inability of MyoD to bind the chromatin at the G 2 phase of the cell cycle. These results indicate an intimate relationship between DNA damage-activated cell cycle checkpoints and the control of tissue-specific gene expression to allow DNA repair in myoblasts prior to the activation of the differentiation program.
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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 OpenQuestion graph.