ReviewJournal of cellular physiology2010
Core binding factor at the crossroads: determining the fate of the HSC.
Review in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- High-risk cytogenetic abnormalities impact the cytological and clinical behavior of core binding factor acute myeloid leukemia: a case-control study.BMC cancer · 2026Article
- TAF1 is required for fetal but not adult hematopoiesis in mice.Developmental cell · 2025Article
- The Functional and Prognostic Impact of TIGIT Expression on Bone Marrow NK Cells in Core Binding Factor-Acute Myeloid Leukemia Patients at Diagnosis.Biomedicines · 2024Article
- Article
- Proteomic Analysis of Murine Bone Marrow Very Small Embryonic-like Stem Cells at Steady-State Conditions and after In Vivo Stimulation by Nicotinamide and Follicle-Stimulating Factor Reflects their Germ-Lineage Origin and Multi Germ Layer Differentiation Potential.Stem cell reviews and reports · 2023Article
- Core binding factor subunit β plays diverse and essential roles in the male germline.Frontiers in cell and developmental biology · 2023Article
- Review
- Article
- Review
- 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
- RUNX3-dependent oxidative epithelial-to-mesenchymal transition in methamphetamine-induced chronic lung injury.Cell stress & chaperones · 2020Article
- MicroRNAs and lncRNAs-A New Layer of Myeloid-Derived Suppressor Cells Regulation.Frontiers in immunology · 2020Review
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- Profiling the epigenetic interplay of lncRNA RUNXOR and oncogenic RUNX1 in breast cancer cells by gene in situ cis-activation.American journal of cancer research · 2019Article
- Identification of Key Genes and Pathways Associated with RUNX1 Mutations in Acute Myeloid Leukemia Using Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Loss ofOpen biology · 2018Article
- Article
- The ubiquitin ligase STUB1 regulates stability and activity of RUNX1 and RUNX1-RUNX1T1.The Journal of biological chemistry · 2017Article
- Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Small Molecule Inhibitor of CBFβ-RUNX Binding for RUNX Transcription Factor Driven Cancers.EBioMedicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hematopoietic development requires coordinated actions from a variety of transcription factors. The core binding factor (CBF), consisting of a Runx protein and the CBFbeta protein, is a transcription factor complex that is essential for emergence of the hematopoietic stem cell (HSC) from an endothelial cell stage. The hematopoietic defects observed in either Runx1 or CBFbeta knockout mice underscore the necessity of this complex for definitive hematopoiesis. Despite the requirement for CBF in establishing definitive hematopoiesis, Runx1 loss has minimal impact on maintaining the HSC state postnatally, while CBFbeta may continue to be essential. Lineage commitment, on the other hand, is significantly affected upon CBF loss in the adult, indicating a primary role for this complex in modulating differentiation. Given the impact of normal CBF function in the hematopoietic system, the severe consequences of disrupting CBF activity, either through point mutations or generation of fusion genes, are obvious. The physiologic role of CBF in differentiation is subverted to an active process of self-renewal maintenance by the genetic aberrations, through several possible mechanisms, contributing to the development of hematopoietic malignancies including myelodysplastic syndrome and leukemia. The major impact of CBF on the hematopoietic system in both development and disease highlights the need for understanding the intricate functions of this complex and reiterate the necessity of continued efforts to identify potential points of therapeutic intervention for CBF-related diseases.
Indexed as
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What OpenQuestion holds
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.