ArticleNature communications2020
Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed.
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- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- A common 19 bp APOE enhancer deletion is protective against Alzheimer's disease in African Americans.Nature communications · 2026Article
- The response to kidney injury is epigenetically regulated through the activation of bivalent genes.American journal of physiology. Renal physiology · 2026Article
- PU.1 inhibition sensitizes stem-monocytic AML to BCL2 blockade.bioRxiv : the preprint server for biology · 2026Article
- Genetic variation shapes the chromatin accessibility landscape and transcriptional responses in mouse adipose tissue.PLoS genetics · 2026Article
- Therapeutic targeting SPI1 in combination with erastin promotes ferroptosis in ccRCC.Communications biology · 2025Article
- Article
- Multiomic analyses on the contribution of transposable elements to the cis-regulatory landscape of different types of immune cells.BMC genomics · 2025Article
- DNA bendability regulates transcription factor binding to nucleosomes.Nature structural & molecular biology · 2025Article
- GATA2 decommissioning of enhancers: A mechanism to constrain inflammatory signaling.Cell reports · 2025Article
- Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity.Nature genetics · 2025Article
- Unveiling genetic signatures of immune response in immune-related diseases through single-cell eQTL analysis across diverse conditions.Nature communications · 2025Article
- SUMO operates from a unique long tandem repeat to keep innate immunity in check.Nucleic acids research · 2025Article
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Establishing gene regulatory networks during differentiation or reprogramming requires master or pioneer transcription factors (TFs) such as PU.1, a prototype master TF of hematopoietic lineage differentiation. To systematically determine molecular features that control its activity, here we analyze DNA-binding in vitro and genome-wide in vivo across different cell types with native or ectopic PU.1 expression. Although PU.1, in contrast to classical pioneer factors, is unable to access nucleosomal target sites in vitro, ectopic induction of PU.1 leads to the extensive remodeling of chromatin and redistribution of partner TFs. De novo chromatin access, stable binding, and redistribution of partner TFs both require PU.1's N-terminal acidic activation domain and its ability to recruit SWI/SNF remodeling complexes, suggesting that the latter may collect and distribute co-associated TFs in conjunction with the non-classical pioneer TF PU.1.
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