ArticleNature2013
A stable transcription factor complex nucleated by oligomeric AML1-ETO controls leukaemogenesis.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 162 citations in OpenAlex.
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- CBFA2T2: a novel H3K27 reader regulating metabolism and tumor growth.Molecular cancer · 2026Article
- HSCs/MPPs as cells of origin with altered differentiation hierarchy impairing immunomicroenvironment inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- 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
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 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
- Identification of non-charged 7.44 analogs interacting with the NHR2 domain of RUNX1-ETO with improved antiproliferative effect in RUNX-ETO positive cells.Scientific reports · 2025Article
- Acute resistance to BET inhibitors remodels compensatory transcriptional programs via p300 coactivation.Blood · 2025Article
- Catalytic activity of Setd2 is essential for embryonic development in mice: establishment of a mouse model harboring patient-derived Setd2 mutation.Frontiers of medicine · 2024Article
- Article
- Distinct phases of cellular signaling revealed by time-resolved protein synthesis.Nature chemical biology · 2024Article
- Combination of eriocalyxin B and homoharringtonine exerts synergistic anti-tumor effects against t(8;21) AML.Acta pharmacologica Sinica · 2024Article
- A novel AML1-ETO/FTO positive feedback loop promotes leukemogenesis and Ara-C resistance via stabilizing IGFBP2 in t(8;21) acute myeloid leukemia.Experimental hematology & oncology · 2024Article
- BloodChIP Xtra: an expanded database of comparative genome-wide transcription factor binding and gene-expression profiles in healthy human stem/progenitor subsets and leukemic cells.Nucleic acids research · 2024Article
- The non-cell-autonomous function of ID1 promotes AML progression via ANGPTL7 from the microenvironment.Blood · 2023Article
- LMO2 promotes the development of AML through interaction with transcription co-regulator LDB1.Cell death & disease · 2023Article
- A systematic survey of LU domain-containing proteins reveals a novel human gene, LY6A, which encodes the candidate ortholog of mouse Ly-6A/Sca-1 and is aberrantly expressed in pituitary tumors.Frontiers of medicine · 2023Article
- Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Transcription factors are frequently altered in leukaemia through chromosomal translocation, mutation or aberrant expression. AML1-ETO, a fusion protein generated by the t(8;21) translocation in acute myeloid leukaemia, is a transcription factor implicated in both gene repression and activation. AML1-ETO oligomerization, mediated by the NHR2 domain, is critical for leukaemogenesis, making it important to identify co-regulatory factors that 'read' the NHR2 oligomerization and contribute to leukaemogenesis. Here we show that, in human leukaemic cells, AML1-ETO resides in and functions through a stable AML1-ETO-containing transcription factor complex (AETFC) that contains several haematopoietic transcription (co)factors. These AETFC components stabilize the complex through multivalent interactions, provide multiple DNA-binding domains for diverse target genes, co-localize genome wide, cooperatively regulate gene expression, and contribute to leukaemogenesis. Within the AETFC complex, AML1-ETO oligomerization is required for a specific interaction between the oligomerized NHR2 domain and a novel NHR2-binding (N2B) motif in E proteins. Crystallographic analysis of the NHR2-N2B complex reveals a unique interaction pattern in which an N2B peptide makes direct contact with side chains of two NHR2 domains as a dimer, providing a novel model of how dimeric/oligomeric transcription factors create a new protein-binding interface through dimerization/oligomerization. Intriguingly, disruption of this interaction by point mutations abrogates AML1-ETO-induced haematopoietic stem/progenitor cell self-renewal and leukaemogenesis. These results reveal new mechanisms of action of AML1-ETO, and provide a potential therapeutic target in t(8;21)-positive acute myeloid leukaemia.
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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.