ArticleBMC molecular biology2016
Signal transducer and activator of transcription STAT5 is recruited to c-Myc super-enhancer.
Article in BMC molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- An Integrative Drug-Induced Transcriptomic Analysis Identifies Novel MYC Antagonists and Potential Synergistic Drug Combinations.Molecular carcinogenesis · 2025Article
- Targeting senescent stemlike subpopulations in Philadelphia chromosome-like acute lymphoblastic leukemia.Blood · 2025Article
- Bromodomain and extra-terminal proteins in solid tumors: regulators of immune microenvironment and emerging therapeutic targets.Frontiers in immunology · 2025Review
- MYC overexpression in natural killer cell lymphoma: prognostic and therapeutic implications.Haematologica · 2024Article
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- Super-enhancers complexes zoom in transcription in cancer.Journal of experimental & clinical cancer research : CR · 2023Review
- Disruption of the MYC Superenhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia.Molecular cancer research : MCR · 2023Article
- Myc controls NK cell development, IL-15-driven expansion, and translational machinery.Life science alliance · 2023Article
- Metabolic regulation by prostaglandin EAllergy · 2023Article
- STAT1 maintains naïve CD8Science advances · 2021Article
- B-cell acute lymphoblastic leukemia-related microRNAs: uncovering their diverse and special roles.American journal of cancer research · 2021Review
- A novel TLX1-driven T-ALL zebrafish model: comparative genomic analysis with other leukemia models.Leukemia · 2020Article
- SYK inhibition targets acute myeloid leukemia stem cells by blocking their oxidative metabolism.Cell death & disease · 2020Article
- BET Epigenetic Reader Proteins in Cardiovascular Transcriptional Programs.Circulation research · 2020Review
- The combination of BET and PARP inhibitors is synergistic in models of cholangiocarcinoma.Cancer letters · 2020Article
- Comprehensive in vivo identification of the c-Myc mRNA protein interactome using HyPR-MS.RNA (New York, N.Y.) · 2019Article
- The FLT3-ITD mutation and the expression of its downstream signaling intermediates STAT5 and Pim-1 are positively correlated with CXCR4 expression in patients with acute myeloid leukemia.Scientific reports · 2019Article
- Super-enhancers: critical roles and therapeutic targets in hematologic malignancies.Journal of hematology & oncology · 2019Review
- Akt and STAT5 mediate naïve human CD4+ T-cell early metabolic response to TCR stimulation.Nature communications · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundc-Myc has been proposed as a putative target gene of signal transducer and activator of transcription 5 (STAT5). No functional STAT5 binding site has been identified so far within the c-Myc gene locus, therefore a direct transcriptional regulation by STAT5 remains uncertain. c-Myc super-enhancer, located 1.7 Mb downstream of the c-Myc gene locus, was recently reported as essential for the regulation of c-Myc gene expression by hematopoietic transcription factors and bromodomain and extra-terminal (BET) proteins and for leukemia maintenance. c-Myc super-enhancer is composed of five regulatory regions (E1-E5) which recruit transcription and chromatin-associated factors, mediating chromatin looping and interaction with the c-Myc promoter.
resultsWe now show that STAT5 strongly binds to c-Myc super-enhancer regions E3 and E4, both in normal and transformed Ba/F3 cells. We also found that the BET protein bromodomain-containing protein 2 (BRD2), a co-factor of STAT5, co-localizes with STAT5 at E3/E4 in Ba/F3 cells transformed by the constitutively active STAT5-1*6 mutant, but not in non-transformed Ba/F3 cells. BRD2 binding at E3/E4 coincides with c-Myc transcriptional activation and is lost upon treatment with deacetylase and BET inhibitors, both of which inhibit STAT5 transcriptional activity and c-Myc gene expression.
conclusionsOur data suggest that constitutive STAT5 binding to c-Myc super-enhancer might contribute to BRD2 maintenance and thus allow sustained expression of c-Myc in Ba/F3 cells transformed by STAT5-1*6.
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