ArticleCell cycle (Georgetown, Tex.)2012
p53 can repress transcription of cell cycle genes through a p21(WAF1/CIP1)-dependent switch from MMB to DREAM protein complex binding at CHR promoter elements.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.
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Who cites it
81 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Conservation and divergence of the p53 gene regulatory network between mice and humans.Oncogene · 2019Pooled it
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Silencing of MAT2A inhibits gastric cancer cell proliferation, migration, and invasion through activation of the p53 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- CDK2 inhibitor BLU-222 synergizes with CDK4/6 inhibitors in drug resistant breast cancers through p21/p27 induction.Nature communications · 2026Article
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- Potential of Corncob Extract on the Expression of Ki-67 and Caspase3 in Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Therapy-induced senescence of glioblastoma cells is determined by the p21Cell death & disease · 2025Article
- Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres.Cells · 2025Article
- Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres.bioRxiv : the preprint server for biology · 2025Article
- Epstein-Barr virus replication within differentiated epithelia requires pRb sequestration of activator E2F transcription factors.Journal of virology · 2024Article
- A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.Nucleic acids research · 2024Article
- The p21CIP1-CDK4-DREAM axis is a master regulator of genotoxic stress-induced cellular senescence.Nucleic acids research · 2024Article
- Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.Cell communication and signaling : CCS · 2024Article
- Understanding cellular senescence: pathways involved, therapeutics and longevity aiding.Cell cycle (Georgetown, Tex.) · 2023Review
- A systematic approach identifies p53-DREAM pathway target genes associated with blood or brain abnormalities.Disease models & mechanisms · 2023Article
- Exploring the Communication of the SASP: Dynamic, Interactive, and Adaptive Effects on the Microenvironment.International journal of molecular sciences · 2023Review
- Review
- Cell cycle regulation: p53-p21-RB signaling.Cell death and differentiation · 2022Review
21 more citing papers are in PubMed but not listed here.
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Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 plays an important role in cell cycle arrest by downregulating transcription. Many genes repressed by p53 code for proteins with functions in G₂/M. A large portion of these genes is controlled by cell cycle-dependent elements (CDE) and cell cycle genes homology regions (CHR) in their promoters. Cyclin B2 is an example of such a gene, with a function at the transition from G₂ to mitosis. We find that p53-dependent downregulation of cyclin B2 promoter activity is dependent on an intact CHR element. In the presence of high levels of p53 or p21(WAF1/CIP1), protein binding to the CHR switches from MMB to DREAM complex by shifting MuvB core-associated proteins from B-Myb to E2F4/DP1/p130. The results suggest a model for p53-dependent transcriptional repression by which p53 directly activates p21(WAF1/CIP1). The inhibitor then prevents further phosphorylation of p130 by cyclin-dependent kinases. The presence of hypophosphorylated pocket proteins shifts the equilibrium for complex formation from MMB to DREAM. In the case of promoters that do not hold CDE or E2F elements, binding of DREAM and MMB solely relies on a CHR site. Thus, p53 can repress target genes indirectly through CHR elements.
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