ArticleThe EMBO journal1997
p300 is required for MyoD-dependent cell cycle arrest and muscle-specific gene transcription.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
105 citing papers in PubMed, 282 citations in OpenAlex.
- MRG15 decline in aged/injured MuSCs hinders regeneration via differentiation defects.Cell regeneration (London, England) · 2026Article
- MYOD represses gene expression from non-E-box motifs.Genes & development · 2025Article
- E-box independent chromatin recruitment turns MYOD into a transcriptional repressor.bioRxiv : the preprint server for biology · 2024Article
- HDAC inhibitors as pharmacological treatment for Duchenne muscular dystrophy: a discovery journey from bench to patients.Trends in molecular medicine · 2024Review
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- Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex.Nucleic acids research · 2022Article
- p300 arrests intervertebral disc degeneration by regulating the FOXO3/Sirt1/Wnt/β-catenin axis.Aging cell · 2022Article
- Chromatin state distribution of residue-specific histone acetylation in early myoblast differentiation.Journal of big data · 2022Article
- Comparing the epigenetic landscape in myonuclei purified with a PCM1 antibody from a fast/glycolytic and a slow/oxidative muscle.PLoS genetics · 2021Article
- Multi-Omics Approach to Dissect the Mechanisms of Rexinoid Signaling in Myoblast Differentiation.Frontiers in pharmacology · 2021Article
- Chromatin Landscape During Skeletal Muscle Differentiation.Frontiers in genetics · 2020Review
- A Semi-automated Organoid Screening Method Demonstrates Epigenetic Control of Intestinal Epithelial Differentiation.Frontiers in cell and developmental biology · 2020Article
- The Significance of the Intrinsically Disordered Regions for the Functions of the bHLH Transcription Factors.International journal of molecular sciences · 2019Review
- p21cip1/waf1 Coordinate Autophagy, Proliferation and Apoptosis in Response to Metabolic Stress.Cancers · 2019Review
- Germline or inducible knockout of p300 or CBP in skeletal muscle does not alter insulin sensitivity.American journal of physiology. Endocrinology and metabolism · 2019Article
- p300 Mediates Muscle Wasting in Lewis Lung Carcinoma.Cancer research · 2019Article
- CBP and P300 regulate distinct gene networks required for human primary myoblast differentiation and muscle integrity.Scientific reports · 2018Article
- Shaping Gene Expression by Landscaping Chromatin Architecture: Lessons from a Master.Molecular cell · 2018Review
45 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 1 institution in 1 country.
Funding
Abstract
The nuclear phosphoprotein p300 is a new member of a family of 'co-activators' (which also includes the CREB binding protein CBP), that directly modulate transcription by interacting with components of the basal transcriptional machinery. Both p300 and CBP are targeted by the adenovirus E1A protein, and binding to p300 is required for E1A to inhibit terminal differentiation in both keratinocytes and myoblasts. Here we demonstrate that, in differentiating skeletal muscle cells, p300 physically interacts with the myogenic basic helix-loop-helix (bHLH) regulatory protein MyoD at its DNA binding sites. During muscle differentiation, MyoD plays a dual role: besides activating muscle-specific transcription, it induces permanent cell cycle arrest by up-regulating the cyclin-dependent kinase inhibitor p21. We show that p300 is involved in both these activities. Indeed, E1A mutants lacking the ability to bind p300 are greatly impaired in the repression of E-box-driven transcription, and p300 overexpression rescues the wild-type E1A-mediated repression. Moreover, p300 potentiates MyoD- and myogenin-dependent activation of transcription from E-box-containing reporter genes. We also provide evidence, obtained by microinjection of anti-p300 antibodies, that p300 is required for MyoD-dependent cell cycle arrest in either myogenic cells induced to differentiate or in MyoD-converted C3H10T1/2 fibroblasts, but is dispensable for maintenance of the postmitotic state of myotubes.
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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.