ArticleProceedings of the National Academy of Sciences of the United States of America1993
Use of a conditional MyoD transcription factor in studies of MyoD trans-activation and muscle determination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 188 citations in OpenAlex.
- BMP4 derived from human gastrointestinal carcinoma cells impairs myogenic differentiation: A possibleInternational journal of oncology · 2026Article
- Muscle Progenitor Cell Fusion in the Maintenance of Skeletal Muscle.Results and problems in cell differentiation · 2024Article
- Prediabetes-Associated Changes in Skeletal Muscle Function and Their Possible Links with Diabetes: A Literature Review.International journal of molecular sciences · 2023Review
- Pioneer factors in development and cancer.iScience · 2021Review
- Hypoxia preconditioned bone marrow-derived mesenchymal stromal/stem cells enhance myoblast fusion and skeletal muscle regeneration.Stem cell research & therapy · 2021Article
- Design of novel small molecule base-pair recognizers of toxic CUG RNA transcripts characteristics of DM1.Computational and structural biotechnology journal · 2021Article
- Otic Neurogenesis inFrontiers in neuroanatomy · 2021Article
- c-Abl Kinase Is Required for Satellite Cell Function Through Pax7 Regulation.Frontiers in cell and developmental biology · 2021Article
- Post-transcriptional regulation of MRTF-A by miRNAs during myogenic differentiation of myoblasts.Nucleic acids research · 2020Article
- Satellite cells in ageing: use it or lose it.Open biology · 2020Review
- 2-hydroxyglutarate inhibits MyoD-mediated differentiation by preventing H3K9 demethylation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Znf703 is a novel RA target in the neural plate border.Scientific reports · 2019Article
- CRISPR/Cas9-Mediated Deletion of CTG Expansions Recovers Normal Phenotype in Myogenic Cells Derived from Myotonic Dystrophy 1 Patients.Molecular therapy. Nucleic acids · 2017Article
- The muscle regulatory transcription factor MyoD participates with p53 to directly increase the expression of the pro-apoptotic Bcl2 family member PUMA.Apoptosis : an international journal on programmed cell death · 2017Article
- Enhanced Development of Skeletal Myotubes from Porcine Induced Pluripotent Stem Cells.Scientific reports · 2017Article
- Negative regulation of initial steps in skeletal myogenesis by mTOR and other kinases.Scientific reports · 2016Article
- Direct reprogramming of urine-derived cells with inducible MyoD for modeling human muscle disease.Skeletal muscle · 2016Article
- Early neural ectodermal genes are activated by Siamois and Twin during blastula stages.Genesis (New York, N.Y. : 2000) · 2015Article
- A novel role of PRR14 in the regulation of skeletal myogenesis.Cell death & disease · 2015Article
- Dissecting reprogramming, differentiation and conversion with network biology.Leukemia supplements · 2014Article
6 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA sequences encoding the hormone-binding domains of several steroid hormone receptors were fused in frame to the MyoD gene. When the gene for this chimeric protein was expressed in NIH 3T3 or 10T1/2 fibroblasts, these cells displayed hormone-dependent induction of myogenesis. Our experiments focused on cell lines expressing estrogen receptor-MyoD chimeras. Induction of these lines in the presence of estradiol and an inhibitor of protein synthesis, cycloheximide, resulted in the activation of the endogenous myogenin gene but did not activate the muscle-specific creatine kinase or cardiac alpha-actin gene. This result suggests that MyoD is not a "direct" activator of these downstream myogenic genes but must first activate myogenin as an intermediary. Once muscle is induced by estrogen receptor-MyoD the muscle phenotype is very stable and does not need the continued presence of estradiol for its maintenance.
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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.