ArticleBlood2009
Structure of the AML1-ETO eTAFH domain-HEB peptide complex and its contribution to AML1-ETO activity.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- t(8;21)AML patients with RUNX1e6::RUNX1T19a splice variant have poor prognosis.Annals of hematology · 2025Article
- A multi-omic single-cell landscape reveals transcription and epigenetic regulatory features of t(8;21) AML.Journal of translational medicine · 2025Article
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- The role of multivalency in the association of the eight twenty-one protein 2 (ETO2) with the nucleosome remodeling and deacetylase (NuRD) complex.Nucleic acids research · 2025Article
- Recurrent somatic mutations of FAT family cadherins induce an aggressive phenotype and poor prognosis in anaplastic large cell lymphoma.British journal of cancer · 2024Article
- αα-hub coregulator structure and flexibility determine transcription factor binding and selection in regulatory interactomes.The Journal of biological chemistry · 2022Article
- Relationship between the structure and function of the transcriptional regulator E2A.Journal of biological research (Thessalonike, Greece) · 2021Review
- Structural insights into TAZ2 domain-mediated CBP/p300 recruitment by transactivation domain 1 of the lymphopoietic transcription factor E2A.The Journal of biological chemistry · 2020Article
- TAF1 plays a critical role in AML1-ETO driven leukemogenesis.Nature communications · 2019Article
- The CDK7 inhibitor THZ1 alters RNA polymerase dynamics at the 5' and 3' ends of genes.Nucleic acids research · 2019Article
- A tool compound targeting the core binding factor Runt domain to disrupt binding to CBFβ in leukemic cells.Leukemia & lymphoma · 2018Article
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- t(15;21) translocations leading to the concurrent downregulation of RUNX1 and its transcription factor partner genes SIN3A and TCF12 in myeloid disorders.Molecular cancer · 2015Article
- Article
- Targeted cancer exome sequencing reveals recurrent mutations in myeloproliferative neoplasms.Leukemia · 2014Article
- Differential involvement of E2A-corepressor interactions in distinct leukemogenic pathways.Nucleic acids research · 2014Article
- A stable transcription factor complex nucleated by oligomeric AML1-ETO controls leukaemogenesis.Nature · 2013Article
- Myeloid translocation gene 16 is required for maintenance of haematopoietic stem cell quiescence.The EMBO journal · 2012Article
- The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.Science (New York, N.Y.) · 2011Article
- RUNX1 mutations in clonal myeloid disorders: from conventional cytogenetics to next generation sequencing, a story 40 years in the making.Critical reviews in oncogenesis · 2011Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
AML1-ETO is the chimeric protein product of the t(8;21) in acute myeloid leukemia. The ETO portion of the fusion protein includes the eTAFH domain, which is homologous to several TATA binding protein-associated factors (TAFs) and interacts with E proteins (E2A and HEB). It has been proposed that AML1-ETO-mediated silencing of E protein function might be important for t(8;21) leukemogenesis. Here, we determined the solution structure of a complex between the AML1-ETO eTAFH domain and an interacting peptide from HEB. On the basis of the structure, key residues in AML1-ETO for HEB association were mutated. These mutations do not impair the ability of AML1-ETO to enhance the clonogenic capacity of primary mouse bone marrow cells and do not eliminate its ability to repress proliferation or granulocyte differentiation. Therefore, the eTAFH-E protein interaction appears to contribute relatively little to the activity of AML1-ETO.
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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.