ArticlePLoS genetics2008
AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Article
- Nanoparticle-mediated targeting of the fusion gene RUNX1/ETO in t(8;21)-positive acute myeloid leukaemia.Leukemia · 2023Article
- LYL1 facilitates AETFC assembly and gene activation by recruiting CARM1 in t(8;21) AML.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mitochondria and Their Relationship with Common Genetic Abnormalities in Hematologic Malignancies.Life (Basel, Switzerland) · 2021Review
- Zinc finger protein ZNF384 is an adaptor of Ku to DNA during classical non-homologous end-joining.Nature communications · 2021Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- The RUNX1/RUNX1T1 network: translating insights into therapeutic options.Experimental hematology · 2021Review
- RUNX1/RUNX1T1 mediates alternative splicing and reorganises the transcriptional landscape in leukemia.Nature communications · 2021Article
- Nuclear export of chimeric mRNAs depends on an lncRNA-triggered autoregulatory loop in blood malignancies.Cell death & disease · 2020Article
- Differential HDAC1/2 network analysis reveals a role for prefoldin/CCT in HDAC1/2 complex assembly.Scientific reports · 2018Article
- Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Leukemia · 2017Article
- Article
- The miR-23a~27a~24-2 microRNA cluster buffers transcription and signaling pathways during hematopoiesis.PLoS genetics · 2017Article
- A novel epigeneticEMBO molecular medicine · 2017Article
- Suppression of RUNX1/ETO oncogenic activity by a small molecule inhibitor of tetramerization.Haematologica · 2017Article
- AML1/ETO accelerates cell migration and impairs cell-to-cell adhesion and homing of hematopoietic stem/progenitor cells.Scientific reports · 2016Article
- Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Epigenetic Silencing of Eyes Absent 4 Gene by Acute Myeloid Leukemia 1-Eight-twenty-one Oncoprotein Contributes to Leukemogenesis in t(8;21) Acute Myeloid Leukemia.Chinese medical journal · 2016Article
- AML1/ETO cooperates with HIF1α to promote leukemogenesis through DNMT3a transactivation.Leukemia · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
A reciprocal translocation involving chromosomes 8 and 21 generates the AML1/ETO oncogenic transcription factor that initiates acute myeloid leukemia by recruiting co-repressor complexes to DNA. AML1/ETO interferes with the function of its wild-type counterpart, AML1, by directly targeting AML1 binding sites. However, transcriptional regulation determined by AML1/ETO probably relies on a more complex network, since the fusion protein has been shown to interact with a number of other transcription factors, in particular E-proteins, and may therefore target other sites on DNA. Genome-wide chromatin immunoprecipitation and expression profiling were exploited to identify AML1/ETO-dependent transcriptional regulation. AML1/ETO was found to co-localize with AML1, demonstrating that the fusion protein follows the binding pattern of the wild-type protein but does not function primarily by displacing it. The DNA binding profile of the E-protein HEB was grossly rearranged upon expression of AML1/ETO, and the fusion protein was found to co-localize with both AML1 and HEB on many of its regulated targets. Furthermore, the level of HEB protein was increased in both primary cells and cell lines expressing AML1/ETO. Our results suggest a major role for the functional interaction of AML1/ETO with AML1 and HEB in transcriptional regulation determined by the fusion protein.
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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.