ArticleProceedings of the National Academy of Sciences of the United States of America2012
A core erythroid transcriptional network is repressed by a master regulator of myelo-lymphoid differentiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.
- The Effects and Safety of Silymarin on β-thalassemia in Children and Adolescents: A Systematic Review based on Clinical Trial Studies.Reviews on recent clinical trials · 2024Pooled it
- New Insights Into Pathophysiology of β-Thalassemia.Frontiers in medicine · 2022Pooled it
- Metabolic disease variants rewire gene regulation through disruption of DNA G-quadruplex structures.Genome biology · 2026Article
- LDB1 regulates gene expression and chromatin structure in pluripotency and lineage differentiation.Nucleic acids research · 2026Article
- Mixed-model and transcriptome-wide association analyses identify transcription factors and genes associated with colorectal cancer susceptibility.Nature communications · 2026Article
- Canalizing cell fate by transcriptional repression.Molecular systems biology · 2024Review
- Transcription Factor TAL1 in Erythropoiesis.Advances in experimental medicine and biology · 2024Review
- BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state.Nature communications · 2023Article
- Association of DDX5/p68 protein with the upstream erythroid enhancer element (EHS1) of the gene encoding the KLF1 transcription factor.The Journal of biological chemistry · 2023Article
- LinCell proliferation · 2023Article
- Review
- Integrating transcription factor occupancy with transcriptome-wide association analysis identifies susceptibility genes in human cancers.Nature communications · 2022Article
- Identification of transcription factors dictating blood cell development using a bidirectional transcription network-based computational framework.Scientific reports · 2022Article
- HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.Nucleic acids research · 2022Article
- Multiple cell populations generate macrophage progenitors in the early yolk sac.Cellular and molecular life sciences : CMLS · 2022Article
- Identification of the transcription factor MAZ as a regulator of erythropoiesis.Blood advances · 2021Article
- The shifting shape and functional specializations of the cell cycle during lineage development.WIREs mechanisms of disease · 2021Review
- FBXO11-mediated proteolysis of BAHD1 relieves PRC2-dependent transcriptional repression in erythropoiesis.Blood · 2021Article
- Cellular Basis of Embryonic Hematopoiesis and Its Implications in Prenatal Erythropoiesis.International journal of molecular sciences · 2020Review
- Core transcriptional regulatory circuitries in cancer.Oncogene · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Two mechanisms that play important roles in cell fate decisions are control of a "core transcriptional network" and repression of alternative transcriptional programs by antagonizing transcription factors. Whether these two mechanisms operate together is not known. Here we report that GATA-1, SCL, and Klf1 form an erythroid core transcriptional network by co-occupying >300 genes. Importantly, we find that PU.1, a negative regulator of terminal erythroid differentiation, is a highly integrated component of this network. GATA-1, SCL, and Klf1 act to promote, whereas PU.1 represses expression of many of the core network genes. PU.1 also represses the genes encoding GATA-1, SCL, Klf1, and important GATA-1 cofactors. Conversely, in addition to repressing PU.1 expression, GATA-1 also binds to and represses >100 PU.1 myelo-lymphoid gene targets in erythroid progenitors. Mathematical modeling further supports that this dual mechanism of repressing both the opposing upstream activator and its downstream targets provides a synergistic, robust mechanism for lineage specification. Taken together, these results amalgamate two key developmental principles, namely, regulation of a core transcriptional network and repression of an alternative transcriptional program, thereby enhancing our understanding of the mechanisms that establish cellular identity.
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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.