ArticleOncogene2003
Direct association between PU.1 and MeCP2 that recruits mSin3A-HDAC complex for PU.1-mediated transcriptional repression.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 78 citations in OpenAlex.
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- Human microglial cells as a therapeutic target in a neurodevelopmental disease model.Stem cell reports · 2024Article
- Extending MeCP2 interactome: canonical nucleosomal histones interact with MeCP2.Nucleic acids research · 2024Article
- A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation.The Journal of experimental medicine · 2023Article
- Histone Deacetylases Function in the Control of Early Hematopoiesis and Erythropoiesis.International journal of molecular sciences · 2022Review
- Genetics behind Cerebral Disease with Ocular Comorbidity: Finding Parallels between the Brain and Eye Molecular Pathology.International journal of molecular sciences · 2022Review
- Macrophage-targeted delivery of siRNA to silenceBioengineering & translational medicine · 2022Article
- Regulating the Regulators: The Role of Histone Deacetylase 1 (HDAC1) in Erythropoiesis.International journal of molecular sciences · 2020Review
- MeCP2 and Chromatin Compartmentalization.Cells · 2020Review
- Role of HDACs in normal and malignant hematopoiesis.Molecular cancer · 2020Review
- Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications.Frontiers in oncology · 2020Article
- Open Chromatin Profiling in Adipose Tissue Marks Genomic Regions with Functional Roles in Cardiometabolic Traits.G3 (Bethesda, Md.) · 2019Article
- Safeguard function of PU.1 shapes the inflammatory epigenome of neutrophils.Nature immunology · 2019Article
- Old dog PU.1 reveals new tricks.Nature immunology · 2019Article
- Loss of HDAC11 ameliorates clinical symptoms in a multiple sclerosis mouse model.Life science alliance · 2018Article
- PM20D1 is a quantitative trait locus associated with Alzheimer's disease.Nature medicine · 2018Article
- Digging deep into "dirty" drugs - modulation of the methylation machinery.Drug metabolism reviews · 2015Review
- Epigenetics in radiation-induced fibrosis.Oncogene · 2015Review
- Epigenetic Alterations in Alzheimer's Disease.Frontiers in behavioral neuroscience · 2015Review
- PU.1 Suppresses Th2 Cytokine Expression via Silencing of GATA3 Transcription in Dendritic Cells.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PU.1, a member of the Ets family of transcription factors, is implicated in hematopoietic cell differentiation through its interactions with other transcriptional factors and cofactors. To identify a novel protein(s) binding to PU.1, we carried out affinity purification using a column of Glutathione-Sepharose beads bound to GST-PU.1 fusion protein and isolated several individual proteins using murine erythroleukemia (MEL) cell extracts. Sequence analysis of these proteins revealed that one was MeCP2 a methyl CpG binding protein. GST-pull-down assay and immunoprecipitation assay showed that PU.1 bound directly to MeCP2 via its Ets domain and MeCP2 bound to PU.1 via either its amino terminal domain or trans-repression domain. MeCP2 repressed transcriptional activity of PU.1 on a reporter construct with trimerized PU.1 binding sites. This downregulation was recovered in the presence of histone deacetylase inhibitor, trichostatin A (TSA). MeCP2 was integrated in PU.1-mSin3A-HDAC complex but not in PU.1-CBP complex. Chromatin immunoprecipitation (ChIP) assays showed that PU.1 and MeCP2 were collocated at the PU.1 binding site on the reporter construct and the PU.1 binding site of the intervening sequence 2 (IVS2) region in the intron of the beta-globin gene, which has been proposed to regulate expression of the gene, in undifferentiated MEL cells. The complex disappeared from the region during the course of erythroid differentiation of MEL cells. Our results suggest that MeCP2 acts as a corepressor of PU.1 probably due to facilitating complex formation with mSin3A and HDACs.
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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.