ReviewGenes & development2014
Pioneer transcription factors in cell reprogramming.
Review in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 372 papers, 1 of them a synthesis 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.
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Who cites it
372 citing papers in PubMed, 1 synthesis or guideline pooled it, 629 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Endothelial exosomes remodel chromatin accessibility and superenhancer in cancer cells to promote liver metastatic colonization.Signal transduction and targeted therapy · 2026Article
- Fusion Oncoprotein EWSR1::FLI1 Invades Nucleosomes at Consensus ETS Motifs and GGAA Microsatellites.bioRxiv : the preprint server for biology · 2026Article
- Systematic comparison of estimates of transcription factor activity by ATAC-seq and multiplexed reporter assays.Molecular systems biology · 2026Article
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- Article
- Comparative ASCL1 Interactome Analysis Reveals CDK2-Cyclin A2 as Suppressors of Differentiation in MYCN-Amplified Neuroblastoma.Molecular cancer research : MCR · 2026Article
- Ascl1 Represses Müller Glial and Promotes Rod Photoreceptor Fate Through Repressing Notch Signaling in Late Retinal Progenitor Cells.Investigative ophthalmology & visual science · 2026Article
- Asymmetric chromatin accessibility underlies anterior-posterior axis specification in moth fly embryos.PLoS biology · 2026Article
- Pioneer-factor activity requires stable chromatin occupancy mediated by both sequence-specific binding and disordered protein domains.Science advances · 2026Article
- Intrinsic DNA codes govern distinct modes of nucleosome-transcription factor interactions.Nature communications · 2026Article
- Combinatorial pioneer transcription factor binding reinforces bivalent epigenetic states to preserve lineage fidelity.bioRxiv : the preprint server for biology · 2026Article
- H2A.Z facilitates Sox2-nucleosome interaction by promoting DNA and histone H3 tail mobility.Nucleic acids research · 2026Article
- SMARCA4 activation engages FOSL1 to drive enhancer reprogramming and tumorigenic phenotypes in SMARCA4-deficient LUAD cells.Cell death discovery · 2026Article
- SP1 antagonizes H3K27me3 to shape chromatin landscapes for RNA polymerase II recruitment during gastrulation.Nucleic acids research · 2026Article
- SoxB1-mediated chromatin remodeling promotes sensory neuron differentiation in planarians.Genetics · 2026Article
- Genomic perplexity and the evolution of context-dependent function.Molecular biology and evolution · 2026Article
- Redefining cellular reprogramming with advanced genomic technologies.Nature reviews. Genetics · 2026Review
- Fully T2T pedigree assemblies reveal genetic stability and epigenetic plasticity of human centromeres across inheritance and cell-fate transitions.bioRxiv : the preprint server for biology · 2026Article
- SOX2 phosphorylation during mitosis limits genomic damage.Genes & development · 2026Article
312 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
2 authors at 1 institution in 1 country.
Funding
Abstract
A subset of eukaryotic transcription factors possesses the remarkable ability to reprogram one type of cell into another. The transcription factors that reprogram cell fate are invariably those that are crucial for the initial cell programming in embryonic development. To elicit cell programming or reprogramming, transcription factors must be able to engage genes that are developmentally silenced and inappropriate for expression in the original cell. Developmentally silenced genes are typically embedded in "closed" chromatin that is covered by nucleosomes and not hypersensitive to nuclease probes such as DNase I. Biochemical and genomic studies have shown that transcription factors with the highest reprogramming activity often have the special ability to engage their target sites on nucleosomal DNA, thus behaving as "pioneer factors" to initiate events in closed chromatin. Other reprogramming factors appear dependent on pioneer factors for engaging nucleosomes and closed chromatin. However, certain genomic domains in which nucleosomes are occluded by higher-order chromatin structures, such as in heterochromatin, are resistant to pioneer factor binding. Understanding the means by which pioneer factors can engage closed chromatin and how heterochromatin can prevent such binding promises to advance our ability to reprogram cell fates at will and is the topic of this review.
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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.