ArticleProceedings of the National Academy of Sciences of the United States of America1996
Expression of the human acute myeloid leukemia gene AML1 is regulated by two promoter regions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 154 citations in OpenAlex.
- An Isoform-Specific RUNX1C-BTG2 Axis Governs AML Quiescence and Chemoresistance.Blood cancer discovery · 2025Article
- RUNX1A isoform is overexpressed in acute myeloid leukemia and is associated with FLT3 internal tandem duplications.Cancer gene therapy · 2025Article
- RUNX1 isoforms regulate RUNX1 and target genes differentially in platelets-megakaryocytes: association with clinical cardiovascular events.Journal of thrombosis and haemostasis : JTH · 2024Article
- RUNX1 Isoforms Regulate RUNX1 and Target-Genes Differentially in Platelets-Megakaryocytes: Association with Clinical Cardiovascular Events.bioRxiv : the preprint server for biology · 2024Article
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- Age-related promoter-switch regulates Runx1 expression in adult rat hearts.BMC cardiovascular disorders · 2023Article
- RUNX1 isoform disequilibrium promotes the development of trisomy 21-associated myeloid leukemia.Blood · 2023Article
- Review
- Review
- Dynamic Runx1 chromatin boundaries affect gene expression in hematopoietic development.Nature communications · 2022Article
- SON inhibits megakaryocytic differentiation via repressing RUNX1 and the megakaryocytic gene expression program in acute megakaryoblastic leukemia.Cancer gene therapy · 2021Article
- A CRISPR RNA-binding protein screen reveals regulators of RUNX1 isoform generation.Blood advances · 2021Article
- RUNX1: an emerging therapeutic target for cardiovascular disease.Cardiovascular research · 2020Review
- Clinicopathological Significance ofJournal of clinical medicine · 2020Article
- Dysregulation of NIPBL leads to impaired RUNX1 expression and haematopoietic defects.Journal of cellular and molecular medicine · 2020Article
- RUNX1 Dosage in Development and Cancer.Molecules and cells · 2020Review
- The RUNX1 Enhancer Element eR1: A Versatile Marker for Adult Stem Cells.Molecules and cells · 2020Review
- RUNX1-dependent mechanisms in biological control and dysregulation in cancer.Journal of cellular physiology · 2019Review
- Whole-transcriptome splicing profiling of E7.5 mouse primary germ layers reveals frequent alternative promoter usage during mouse early embryogenesis.Biology open · 2018Article
- The transcriptional response to oxidative stress is part of, but not sufficient for, insulin resistance in adipocytes.Scientific reports · 2018Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The human chromosome 21 AML1 gene is expressed predominantly in the hematopoietic system. In several leukemia-associated translocations AML1 is fused to other genes and transcription of the fused regions is mediated by upstream sequences that normally regulate the expression of AML1. The 5' genomic region of AML1 was cloned and sequenced. The two 5' untranslated regions (UTRs) previously identified in AML1 cDNAs were located in this region and the distance between them was established. The distal 5' UTR maps over 7 kb upstream of the proximal one. Using primer extension with mRNA, transcription start sites were identified at two distinct sites above these 5' uTRs. Sequence analysis revealed the absence of a TATA motif and the presence of Sp1, PU.1, Oct, CRE, Myb, Ets, and Ets-like binding sites in both upstream regions. Several initiator elements (Inr) that overlap the transcription start sites were also identified. These proximal and distal upstream regions and their deletion mutants were cloned in front of a luciferase reporter gene and used in transfection assays. We demonstrate that both upstream regions function as promoters in hematopoietic (Jurkat) and nonhematopoietic (HEK) cell lines. The activity of both promoters was orientation dependent and was enhanced, in a cell-type specific manner, by a heterologous enhancer sequence. These results indicate that additional control elements, either negative or positive, regulate the tissue-specific expression of AML1.
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Registered trials
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.