ArticleMolecular and cellular biology2000
Biological characteristics of the leukemia-associated transcriptional factor AML1 disclosed by hematopoietic rescue of AML1-deficient embryonic stem cells by using a knock-in strategy.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 65 citations in OpenAlex.
- Functional analysis of germline RUNX1 variants identified in individuals with suspected familial platelet disorder.Blood advances · 2026Article
- Tumor necrosis factor‑related apoptosis‑inducing ligand is a novel transcriptional target of runt‑related transcription factor 1.International journal of oncology · 2022Article
- CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- RUNX1 regulates site specificity of DNA demethylation by recruitment of DNA demethylation machineries in hematopoietic cells.Blood advances · 2017Article
- Integrated RNA-seq and DNase-seq analyses identify phenotype-specific BMP4 signaling in breast cancer.BMC genomics · 2017Article
- Loss of RUNX1/AML1 arginine-methylation impairs peripheral T cell homeostasis.British journal of haematology · 2015Article
- Long and short non-coding RNAs as regulators of hematopoietic differentiation.International journal of molecular sciences · 2013Review
- Article
- TGF-β superfamily gene expression and induction of the Runx1 transcription factor in adult neurogenic regions after brain injury.PloS one · 2013Article
- 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
- Definitive hematopoiesis requires Runx1 C-terminal-mediated subnuclear targeting and transactivation.Human molecular genetics · 2010Article
- Hematopoietic stem cell emergence in the conceptus and the role of Runx1.The International journal of developmental biology · 2010Review
- Core binding factor at the crossroads: determining the fate of the HSC.Journal of cellular physiology · 2010Review
- Article
- AML1/RUNX1 works as a negative regulator of c-Mpl in hematopoietic stem cells.The Journal of biological chemistry · 2008Article
- Review
- Isoform-specific potentiation of stem and progenitor cell engraftment by AML1/RUNX1.PLoS medicine · 2007Article
- AML1/Runx1 as a versatile regulator of hematopoiesis: regulation of its function and a role in adult hematopoiesis.International journal of hematology · 2006Review
- Review
- Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
AML1 is one of the most frequently mutated genes associated with human acute leukemia and encodes the DNA-binding subunit of the heterodimering transcriptional factor complex, core-binding factor (CBF) (or polyoma enhancer binding protein 2 [PEBP2]). A null mutation in either AML1 or its dimerizing partner, CBFbeta, results in embryonic lethality secondary to a complete block in fetal liver hematopoiesis, indicating an essential role of this transcription complex in the development of definitive hematopoiesis. The hematopoietic phenotype that results from the loss of AML1 can be replicated in vitro with a two-step culture system of murine embryonic stem (ES) cells. Using this experimental system, we now demonstrate that this hematopoietic defect can be rescued by expressing the PEBP2alphaB1 (AML1b) isoform under the endogenous AML1-regulatory sequences through a knock-in (targeted insertion) approach. Moreover, we demonstrate that the rescued AML1(-/-) ES cell clones contribute to lymphohematopoiesis within the context of chimeric animals. Rescue requires the transcription activation domain of AML1 but does not require the C-terminal VWRPY motif, which is conserved in all AML1 family members and has been shown to interact with the transcriptional corepressor, Groucho/transducin-like Enhancer of split. Taken together, these data provide compelling evidence that the phenotype seen in AML1-deficient mice is due solely to the loss of transcriptionally active 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.