ArticleThe Journal of biological chemistry2009
Daxx is a transcriptional repressor of CCAAT/enhancer-binding protein beta.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- The Dynamic Regulation of Daxx-Mediated Transcriptional Inhibition by SUMO and PML NBs.International journal of molecular sciences · 2025Review
- DNA Methylation Changes in Autologous Hematopoietic Stem Cell Transplant Patients.Biological research for nursing · 2023Article
- Gene deficiency or pharmacological inhibition of PDCD4-mediated FGR signaling protects against acute kidney injury.Acta pharmaceutica Sinica. B · 2021Article
- An integrated multi-omics approach identifies epigenetic alterations associated with Alzheimer's disease.Nature genetics · 2020Article
- PTEN in Chromatin Remodeling.Cold Spring Harbor perspectives in medicine · 2020Review
- DAXX promotes ovarian cancer ascites cell proliferation and migration by activating the ERK signaling pathway.Journal of ovarian research · 2018Article
- Article
- PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3.Nature communications · 2017Article
- Signal transducer and activator of transcription 3 regulation by novel binding partners.World journal of biological chemistry · 2015Review
- Death domain-associated protein DAXX promotes ovarian cancer development and chemoresistance.The Journal of biological chemistry · 2013Article
- Berberine represses DAXX gene transcription and induces cancer cell apoptosis.Laboratory investigation; a journal of technical methods and pathology · 2013Article
- Tumor suppressor protein Pdcd4 interacts with Daxx and modulates the stability of Daxx and the Hipk2-dependent phosphorylation of p53 at serine 46.Oncogenesis · 2013Article
- Methylation of RASSF1A gene promoter is regulated by p53 and DAXX.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Death-associated protein 6 (Daxx) mediates cAMP-dependent stimulation of Cyp11a1 (P450scc) transcription.The Journal of biological chemistry · 2012Article
- Transcriptional activation of the adenoviral genome is mediated by capsid protein VI.PLoS pathogens · 2012Article
- Tumor suppressor protein Pdcd4 inhibits translation of p53 mRNA.The Journal of biological chemistry · 2011Article
- Daxx-beta and Daxx-gamma, two novel splice variants of the transcriptional co-repressor Daxx.The Journal of biological chemistry · 2011Article
- Daxx is reciprocally regulated by Mdm2 and Hausp.Biochemical and biophysical research communications · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCAAT/enhancer-binding Protein beta (C/EBPbeta) is a member of the bZIP transcription factor family that is expressed in various tissues, including cells of the hematopoietic system. C/EBPbeta is involved in tissue-specific gene expression and thereby takes part in fundamental cellular processes such as proliferation and differentiation. Here, we show that the activity of C/EBPbeta is negatively regulated by the transcriptional co-repressor Daxx. C/EBPbeta was found to directly interact with Daxx after overexpression as well as on the endogenous level. Glutathione S-transferase pulldown assays showed that Daxx binds via amino acids 190-400 to the C-terminal part of C/EBPbeta. Co-expression of C/EBPbeta changed the sub-nuclear Daxx distribution pattern from predominantly POD-localized to nucleoplasmic. Daxx suppressed basal and p300-enhanced transcriptional activity of C/EBPbeta. Furthermore, Daxx decreased the C/EBPbeta-dependent phosphorylation of p300, which in turn was associated with a diminished level of p300-mediated C/EBPbeta acetylation. Co-expression of promyelocytic leukemia protein abrogated the repressive effect of Daxx on C/EBPbeta as well as the direct interaction of Daxx and C/EBPbeta, presumably by re-recruiting Daxx to PML-oncogenic domains. In acute promyelocytic leukemia (APL) cells, C/EBPbeta activity is known to be required for all-trans-retinoic acid-induced cell differentiation and disease remission. We show that all-trans-retinoic acid as well as arsenic trioxide treatment leads to a reduced C/EBPbeta fraction associated with Daxx suggesting a relief of Daxx-dependent C/EBPbeta repression as an important molecular event leading to APL cell differentiation. Overall, our data identify Daxx as a new negative regulator of C/EBPbeta and provide first clues for a link between abrogation of Daxx-C/EBPbeta complex formation and APL remission.
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