ArticleNucleic acids research2015
Deacetylase inhibitors repress STAT5-mediated transcription by interfering with bromodomain and extra-terminal (BET) protein function.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Martinostat as a novel HDAC inhibitor to overcome tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Clinical epigenetics · 2025Article
- Bromodomain and extra-terminal proteins in solid tumors: regulators of immune microenvironment and emerging therapeutic targets.Frontiers in immunology · 2025Review
- Reduction of class I histone deacetylases ameliorates ER-mitochondria cross-talk in Alzheimer's disease.Aging cell · 2023Article
- STAT5 does not drive steroid resistance in T-cell acute lymphoblastic leukemia despite the activation ofHaematologica · 2023Article
- Molecular profiling and specific targeting of gemcitabine-resistant subclones in heterogeneous pancreatic cancer cell populations.Frontiers in oncology · 2023Article
- Article
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
- Bromodomain and Extraterminal Inhibition by JQ1 Produces Divergent Transcriptional Regulation of Suppressors of Cytokine Signaling Genes in Adipocytes.Endocrinology · 2020Article
- Review
- Biophysical regulation of macrophages in health and disease.Journal of leukocyte biology · 2019Review
- Inhibition of BET Proteins and Histone Deacetylase (HDACs): Crossing Roads in Cancer Therapy.Cancers · 2019Review
- Targeting bromodomain and extraterminal proteins in breast cancer.Pharmacological research · 2018Review
- Dectin-1 Positive Dendritic Cells Expand after Infection withFrontiers in immunology · 2018Article
- The histone deacetylase inhibitor givinostat (ITF2357) exhibits potent anti-tumor activity against CRLF2-rearranged BCP-ALL.Leukemia · 2017Article
- MYC Deregulation in Primary Human Cancers.Genes · 2017Review
- Histone H1 and Chromosomal Protein HMGN2 Regulate Prolactin-induced STAT5 Transcription Factor Recruitment and Function in Breast Cancer Cells.The Journal of biological chemistry · 2017Article
- BET bromodomain proteins and epigenetic regulation of inflammation: implications for type 2 diabetes and breast cancer.Cellular and molecular life sciences : CMLS · 2017Review
- Signal transducer and activator of transcription STAT5 is recruited to c-Myc super-enhancer.BMC molecular biology · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription STAT5 is essential for the regulation of proliferation and survival genes. Its activity is tightly regulated through cytokine signaling and is often upregulated in cancer. We showed previously that the deacetylase inhibitor trichostatin A (TSA) inhibits STAT5-mediated transcription by preventing recruitment of the transcriptional machinery at a step following STAT5 binding to DNA. The mechanism and factors involved in this inhibition remain unknown. We now show that deacetylase inhibitors do not target STAT5 acetylation, as we initially hypothesized. Instead, they induce a rapid increase in global histone acetylation apparently resulting in the delocalization of the bromodomain and extra-terminal (BET) protein Brd2 and of the Brd2-associated factor TBP to hyperacetylated chromatin. Treatment with the BET inhibitor (+)-JQ1 inhibited expression of STAT5 target genes, supporting a role of BET proteins in the regulation of STAT5 activity. Accordingly, chromatin immunoprecipitation demonstrated that Brd2 is associated with the transcriptionally active STAT5 target gene Cis and is displaced upon TSA treatment. Our data therefore indicate that Brd2 is required for the proper recruitment of the transcriptional machinery at STAT5 target genes and that deacetylase inhibitors suppress STAT5-mediated transcription by interfering with Brd2 function.
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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.