ArticleGenes & development2005
Runx1 prevents wasting, myofibrillar disorganization, and autophagy of skeletal muscle.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
What it found
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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.
The trial behind it
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Who cites it
104 citing papers in PubMed, 174 citations in OpenAlex.
- The impact of postexercise essential amino acid ingestion on the ubiquitin proteasome and autophagosomal-lysosomal systems in skeletal muscle of older men.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Trial
- RUNX transcription factors: association with pediatric asthma and modulated by maternal smoking.American journal of physiology. Lung cellular and molecular physiology · 2011Trial
- A Hypertrophic Stimulus Drives Age-Dependent Transcript Isoform Switching With and Without Differential Gene Expression in Skeletal Muscle.Aging cell · 2026Article
- The Age-Dependent Resident Myonuclear Multi-Omic Response to an Acute Skeletal Muscle Hypertrophic Stimulus in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-Nucleus RNA Sequencing Reveals Muscle Fiber Cell Heterogeneity During Human Skeletal Muscle Aging.Aging cell · 2026Article
- Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia.American journal of physiology. Cell physiology · 2026Article
- The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus.bioRxiv : the preprint server for biology · 2025Article
- Article
- Establishment and characterization of novel cancer cachexia-inducing cell line, Aku60GC, of scirrhous gastric cancer.Human cell · 2025Article
- Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy.Cell proliferation · 2025Article
- Hormesis and Muscle Plasticity.Advances in experimental medicine and biology · 2025Review
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth.EMBO reports · 2024Article
- Time-series transcriptomics reveals distinctive mRNA expression dynamics associated with gene ontology specificity and protein expression in skeletal muscle after electrical stimulation-induced resistance exercise.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Contractile regulation of the glucocorticoid-sensitive transcriptome in young and aged skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2024Article
- Restoring Skeletal Muscle Health through Exercise in Breast Cancer Patients and after Receiving Chemotherapy.International journal of molecular sciences · 2024Review
- Article
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle ImplicatesbioRxiv : the preprint server for biology · 2024Article
- Therapeutic Targeting of the GSK3β-CUGBP1 Pathway in Myotonic Dystrophy.International journal of molecular sciences · 2023Article
- Transcriptomic and Proteomic of Gastrocnemius Muscle in Peripheral Artery Disease.Circulation research · 2023Article
- Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Disruptions in the use of skeletal muscle lead to muscle atrophy. After short periods of disuse, muscle atrophy is reversible, and even after prolonged periods of inactivity, myofiber degeneration is uncommon. The pathways that regulate atrophy, initiated either by peripheral nerve damage, immobilization, aging, catabolic steroids, or cancer cachexia, however, are poorly understood. Previously, we found that Runx1 (AML1), a DNA-binding protein that is homologous to Drosophila Runt and has critical roles in hematopoiesis and leukemogenesis, is poorly expressed in innervated muscle, but strongly induced in muscle shortly after denervation. To determine the function of Runx1 in skeletal muscle, we generated mice in which Runx1 was selectively inactivated in muscle. Here, we show that Runx1 is required to sustain muscle by preventing denervated myofibers from undergoing myofibrillar disorganization and autophagy, structural defects found in a variety of congenital myopathies. We find that only 29 genes, encoding ion channels, signaling molecules, and muscle structural proteins, depend upon Runx1 expression, suggesting that their misregulation causes the dramatic muscle wasting. These findings demonstrate an unexpected role for electrical activity in regulating muscle wasting, and indicate that muscle disuse induces compensatory mechanisms that limit myofiber atrophy. Moreover, these results suggest that reduced muscle activity could cause or contribute to congenital myopathies if Runx1 or its target genes were compromised.
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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.