ArticleOncogene2001
In vivo complex formation of PU.1 with HDAC1 associated with PU.1-mediated transcriptional repression.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- HDAC6 regulates human erythroid differentiation through modulation of JAK2 signalling.Journal of cellular and molecular medicine · 2023Article
- HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.Nucleic acids research · 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
- PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.The Journal of experimental medicine · 2021Article
- Regulating the Regulators: The Role of Histone Deacetylase 1 (HDAC1) in Erythropoiesis.International journal of molecular sciences · 2020Review
- Strategies to generate functionally normal neutrophils to reduce infection and infection-related mortality in cancer chemotherapy.Pharmacology & therapeutics · 2019Review
- 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
- Modeling the Hematopoietic Landscape.Frontiers in cell and developmental biology · 2019Review
- BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia.Haematologica · 2018Article
- Digging deep into "dirty" drugs - modulation of the methylation machinery.Drug metabolism reviews · 2015Review
- PU.1 Suppresses Th2 Cytokine Expression via Silencing of GATA3 Transcription in Dendritic Cells.PloS one · 2015Article
- Extensive remodeling of DC function by rapid maturation-induced transcriptional silencing.Nucleic acids research · 2014Article
- Article
- Metallothionein-1 isoforms and vimentin are direct PU.1 downstream target genes in leukemia cells.The Journal of biological chemistry · 2010Article
- Spi-B inhibits human plasma cell differentiation by repressing BLIMP1 and XBP-1 expression.Blood · 2008Article
- Genetic determination of the role of PU.1 in macrophage gene expression.Biochemical and biophysical research communications · 2008Article
- Dynamic protein associations define two phases of IL-1beta transcriptional activation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Role of hypoxia in the regulation of periovulatory EDN2 expression in the mouse.Canadian journal of physiology and pharmacology · 2008Article
- Cooperative interaction between ETS1 and GFI1 transcription factors in the repression of Bax gene expression.Oncogene · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that overexpression of PU.1, a member of the Ets family of transcription factors, induces differentiation inhibition and apoptosis associated with c-Myc down-regulation in murine erythroleukemia (MEL) cells. To understand the molecular mechanism by which c-Myc is down-regulated due to overexpression of PU.1, we performed luciferase reporter assays using the mouse c-myc promoter. PU.1 repressed the activities of not only the c-myc promoter but also several other promoters. Experiments with deletion mutants of PU.1 revealed that the C-terminal region spanning amino acids (aa) 123-272 including the PEST and ETS domains but not the activation domain was sufficient for this transcriptional repression. It was unlikely that the repression was due to sequestration of a limited amount of CBP/p300 nor pCAF, because overexpression of these co-activators did not relieve PU.1-mediated transcriptional repression. Instead, it was found that the C-terminal aa 101-272 of PU.1 formed a complex with mSin3A and HDAC1 in vivo, which was speculated to be associated with the repression. The C-terminal region of PU.1 also formed a complex with the basic transcription factor TBP in vitro and in vivo. Our results suggest that overexpression of PU.1 induces transcriptional repression in several gene promoters including the c-myc promoter which may be mediated by its complex formation with 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.