ArticleMolecular and cellular biology1999
Activated notch inhibits myogenic activity of the MADS-Box transcription factor myocyte enhancer factor 2C.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy.Frontiers in bioengineering and biotechnology · 2020Pooled it
- miR-203, a tumor suppressor frequently down-regulated by promoter hypermethylation in rhabdomyosarcoma.The Journal of biological chemistry · 2014Trial
- Nanotechnology-mediated strategies for skeletal muscle repair and regeneration: targeted intervention, functional remodeling, and translational challenges.Journal of nanobiotechnology · 2026Review
- Cellular reprogramming of fibroblasts in heart regeneration.Journal of molecular and cellular cardiology · 2023Review
- MEF2C opposes Notch in lymphoid lineage decision and drives leukemia in the thymus.JCI insight · 2022Article
- Regulatory Role of N6-Methyladenosine in Longissimus Dorsi Development in Yak.Frontiers in veterinary science · 2022Article
- MiRNAs and Muscle Regeneration: Therapeutic Targets in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2021Review
- Selective breeding modifies mef2ca mutant incomplete penetrance by tuning the opposing Notch pathway.PLoS genetics · 2019Article
- Region-Restrict Astrocytes Exhibit Heterogeneous Susceptibility to Neuronal Reprogramming.Stem cell reports · 2019Article
- Integrated Analyses Reveal Overexpressed Notch1 Promoting Porcine Satellite Cells' Proliferation through Regulating the Cell Cycle.International journal of molecular sciences · 2018Article
- Antagonistic regulation of cell-cycle and differentiation gene programs in neonatal cardiomyocytes by homologous MEF2 transcription factors.The Journal of biological chemistry · 2017Article
- Notch Inhibition Enhances Cardiac Reprogramming by Increasing MEF2C Transcriptional Activity.Stem cell reports · 2017Article
- Regulation of muscle growth and regeneration by the immune system.Nature reviews. Immunology · 2017Review
- miR-142-3p Contributes to Early Cardiac Fate Decision of Embryonic Stem Cells.Stem cells international · 2017Article
- The role of sex steroid hormones in the pathophysiology and treatment of sarcopenia.Osteoporosis and sarcopenia · 2016Review
- The epigenetic regulation of embryonic myogenesis and adult muscle regeneration by histone methylation modification.Biochemistry and biophysics reports · 2016Review
- Lkb1 deletion upregulates Pax7 expression through activating Notch signaling pathway in myoblasts.The international journal of biochemistry & cell biology · 2016Article
- Notch signaling represses GATA4-induced expression of genes involved in steroid biosynthesis.Reproduction (Cambridge, England) · 2015Article
- Alternative splicing of MEF2C pre-mRNA controls its activity in normal myogenesis and promotes tumorigenicity in rhabdomyosarcoma cells.The Journal of biological chemistry · 2015Article
- Myocyte enhancer factor 2C in hematopoiesis and leukemia.Oncogene · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle gene expression is dependent on combinatorial associations between members of the MyoD family of basic helix-loop-helix (bHLH) transcription factors and the myocyte enhancer factor 2 (MEF2) family of MADS-box transcription factors. The transmembrane receptor Notch interferes with the muscle-inducing activity of myogenic bHLH proteins, and it has been suggested that this inhibitory activity of Notch is directed at an essential cofactor that recognizes the DNA binding domains of the myogenic bHLH proteins. Given that MEF2 proteins interact with the DNA binding domains of myogenic bHLH factors to cooperatively regulate myogenesis, we investigated whether members of the MEF2 family might serve as targets for the inhibitory effects of Notch on myogenesis. We show that a constitutively activated form of Notch specifically blocks DNA binding by MEF2C, as well as its ability to cooperate with MyoD and myogenin to activate myogenesis. Responsiveness to Notch requires a 12-amino-acid region of MEF2C immediately adjacent to the DNA binding domain that is unique to this MEF2 isoform. Two-hybrid assays and coimmunoprecipitations show that this region of MEF2C interacts directly with the ankyrin repeat region of Notch. These findings reveal a novel mechanism for Notch-mediated inhibition of myogenesis and demonstrate that the Notch signaling pathway can discriminate between different members of the MEF2 family.
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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.