ArticleOncogene2006
Site-specific DNA methylation by a complex of PU.1 and Dnmt3a/b.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
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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
62 citing papers in PubMed.
- Selective disruption of DNMT1/ELK1 interactions induces DGKI re-expression and promotes temozolomide sensitivity of MGMTClinical epigenetics · 2025Article
- ATRX ADD domain is a versatile module for recognizing macroH2A, H3, and beyond.Acta biochimica et biophysica Sinica · 2025Article
- The power and the promise of epigenetic drugs in oncology.Frontiers in genetics · 2025Review
- DNMT3B overexpression downregulates genes with CpG islands, common motifs, and transcription factor binding sites that interact with DNMT3B.Scientific reports · 2022Article
- CA10 is associated with HBV-related hepatocarcinogenesis.Biochemistry and biophysics reports · 2022Article
- Fine-grained investigation of the relationship between human nutrition and global DNA methylation patterns.European journal of nutrition · 2022Article
- SPI1-induced downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner.Molecular therapy. Nucleic acids · 2022Article
- Tumor suppressor CEBPA interacts with and inhibits DNMT3A activity.Science advances · 2022Article
- Enzymology of Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
- Deciphering the genetic code of DNA methylation.Briefings in bioinformatics · 2021Review
- B1a and B2 cells are characterized by distinct CpG modification states at DNMT3A-maintained enhancers.Nature communications · 2021Article
- Targeting Epigenetic Mechanisms in Vascular Aging.Frontiers in cardiovascular medicine · 2021Review
- The methylation landscape and its role in domestication and gene regulation in the chicken.Nature ecology & evolution · 2020Article
- Review
- From 1957 to Nowadays: A Brief History of Epigenetics.International journal of molecular sciences · 2020Review
- DNA methyltransferases in hematological malignancies.Journal of genetics and genomics = Yi chuan xue bao · 2020Review
- Association of CNVs with methylation variation.NPJ genomic medicine · 2020Article
- Sensitivity of transcription factors to DNA methylation.Essays in biochemistry · 2019Review
- Open Chromatin Profiling in Adipose Tissue Marks Genomic Regions with Functional Roles in Cardiometabolic Traits.G3 (Bethesda, Md.) · 2019Article
- Human monocyte-to-macrophage differentiation involves highly localized gain and loss of DNA methylation at transcription factor binding sites.Epigenetics & chromatin · 2019Article
2 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ets transcription factor PU.1 is a hematopoietic master regulator essential for the development of myeloid and B-cell lineages. As we previously reported, PU.1 sometimes represses transcription on forming a complex with mSin3A-histone deacetyl transferase-MeCP2. Here, we show an interaction between PU.1 and DNA methyltransferases, DNA methyltransferase (Dnmt)3a and Dnmt3b (Dnmt3s). Glutathione-S-transferase pulldown assay revealed that PU.1 directly interacted with the ATRX domain of Dnmt3s through the ETS domain. Dnmt3s repressed the transcriptional activity of PU.1 on a reporter construct with trimerized PU.1-binding sites. The repression was recovered by addition of 5-aza-deoxycitidine, a DNA methyltransferase inhibitor, but not trichostatin A, a histone deacetylase inhibitor. Bisulfite sequence analysis revealed that several CpG sites in the promoter region neighboring the PU.1-binding sites were methylated when Dnmt3s were coexpressed with PU.1. We also showed that the CpG sites in the p16(INK4A) promoter were methylated by overexpression of PU.1 in NIH3T3 cells, accompanied by a downregulation of p16(INK4A) gene expression. These results suggest that PU.1 may downregulate its target genes through an epigenetic modification such as DNA methylation.
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Registered trials
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