ArticleOncogene2006
ELA2 is regulated by hematopoietic transcription factors, but not repressed by AML1-ETO.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Senescence-associated lineage-aberrant plasticity evokes T-cell-mediated tumor control.Nature communications · 2025Article
- Multidimensional study of the heterogeneity of leukemia cells in t(8;21) acute myelogenous leukemia identifies the subtype with poor outcome.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1.Nucleic acids research · 2018Article
- Pharmacological inhibition of the transcription factor PU.1 in leukemia.The Journal of clinical investigation · 2017Article
- Genome-wide co-occupancy of AML1-ETO and N-CoR defines the t(8;21) AML signature in leukemic cells.BMC genomics · 2015Article
- DNA Microarray Analysis on the Genes Differentially Expressed in the Liver of the Pufferfish, Takifugu rubripes, Following an Intramuscular Administration of Tetrodotoxin.Microarrays (Basel, Switzerland) · 2014Article
- AML1-ETO targets and suppresses cathepsin G, a serine protease, which is able to degrade AML1-ETO in t(8;21) acute myeloid leukemia.Oncogene · 2013Article
- Two distinct auto-regulatory loops operate at the PU.1 locus in B cells and myeloid cells.Blood · 2011Article
- Article
- Crosstalk between C/EBPbeta phosphorylation, arginine methylation, and SWI/SNF/Mediator implies an indexing transcription factor code.The EMBO journal · 2010Article
- G9a-mediated lysine methylation alters the function of CCAAT/enhancer-binding protein-beta.The Journal of biological chemistry · 2008Article
- T-lymphoid, megakaryocyte, and granulocyte development are sensitive to decreases in CBFbeta dosage.Blood · 2007Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 117 bp fragment of the human ELA2 promoter has been characterized that can act as a minimal promoter for the expression of neutrophil elastase. Chromatin immunoprecipitation and siRNAs revealed that expression of ELA2 is regulated by the acute myeloid human leukemia 1 protein (AML1), C/EBPalpha, PU.1 and c-Myb transcription factors. ELA2 has also been investigated as a possible target of the leukemic fusion protein AML1-ETO resulting from the t(8;21) chromosomal translocation. AML1-ETO, like AML1, binds the ELA2 promoter in the myeloid cell lines Kasumi-1 and U937, but unexpectedly fails to significantly alter expression of ELA2. Although AML1-ETO downregulates the expression of C/EBPalpha, changes in C/EBPalpha expression do not correlate with changes in the expression of ELA2. Our observations indicate that AML1-ETO may not be a constitutive repressor of gene expression in every case in which it can associate with DNA, either on its own or in conjunction with C/EBPalpha. Since neither ETO nor AML1-ETO are typically expressed in hematopoietic progenitors, we hypothesize that it is the interactions between AML1-ETO and regulatory cofactors in disease-state cells that alter gene expression programs during hematopoiesis. These protein-protein interactions may not require simultaneous DNA binding by AML1-ETO for the deleterious effects of the fusion protein to be realized.
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