ArticleNature2012
Chromatin-modifying enzymes as modulators of reprogramming.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 391 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
391 citing papers in PubMed, 2 syntheses or guidelines pooled it, 632 citations in OpenAlex.
- Chemical transdifferentiation of somatic cells to neural cells: a systematic review.Einstein (Sao Paulo, Brazil) · 2024Pooled it
- Pluripotent stem cells: induction and self-renewal.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Pooled it
- Depletion of the isocitrate dehydrogenase 3 subunit IDHA-1 licenses germ cell-to-neuron direct reprogramming.bioRxiv : the preprint server for biology · 2026Article
- Review
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- The AT-HOOK MOTIF CONTAINING NUCLEAR LOCALIZED gene promotes somatic embryogenesis and polyploidy formation in Liriodendron hybrids.Plant cell reports · 2026Article
- Trans-histone crosstalk establishes distinct H3K79 methylation zones with differential transcriptional functions.Nucleic acids research · 2026Article
- DOT1L provides transcriptional memory through PRC1.1 antagonism.Nature cell biology · 2026Article
- Human iPSCs derived from cryopreserved testicular somatic cells enable germline regeneration in childhood cancer survivors.Human reproduction open · 2026Article
- Article
- Advances in Induced Pluripotent Stem Cell Reprogramming and Its Application in Amyotrophic Lateral Sclerosis: A Review.FASEB bioAdvances · 2025Review
- Molecular basis of cell fate plasticity - insights from the privileged cells.Current opinion in genetics & development · 2025Review
- Review
- Chemical-based epigenetic reprogramming to advance pluripotency and totipotency.Nature chemical biology · 2025Review
- Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025Review
- A chromatin-focused CRISPR screen identifies USP22 as a barrier to somatic cell reprogramming.Communications biology · 2025Article
- Interplay between pioneer transcription factors and epigenetic modifiers in cell reprogramming.Regenerative therapy · 2025Review
- Chromatin environment-dependent effects of DOT1L on gene expression in male germ cells.Communications biology · 2025Article
- Inducing Pluripotency in Somatic Cells: Historical Perspective and Recent Advances.International journal of stem cells · 2024Review
- A cytoplasmic form of EHMT1N methylates viral proteins to enable inclusion body maturation and efficient viral replication.PLoS biology · 2024Article
331 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
13 authors at 8 institutions in 3 countries.
Funding
Abstract
Generation of induced pluripotent stem cells (iPSCs) by somatic cell reprogramming involves global epigenetic remodelling. Whereas several proteins are known to regulate chromatin marks associated with the distinct epigenetic states of cells before and after reprogramming, the role of specific chromatin-modifying enzymes in reprogramming remains to be determined. To address how chromatin-modifying proteins influence reprogramming, we used short hairpin RNAs (shRNAs) to target genes in DNA and histone methylation pathways, and identified positive and negative modulators of iPSC generation. Whereas inhibition of the core components of the polycomb repressive complex 1 and 2, including the histone 3 lysine 27 methyltransferase EZH2, reduced reprogramming efficiency, suppression of SUV39H1, YY1 and DOT1L enhanced reprogramming. Specifically, inhibition of the H3K79 histone methyltransferase DOT1L by shRNA or a small molecule accelerated reprogramming, significantly increased the yield of iPSC colonies, and substituted for KLF4 and c-Myc (also known as MYC). Inhibition of DOT1L early in the reprogramming process is associated with a marked increase in two alternative factors, NANOG and LIN28, which play essential functional roles in the enhancement of reprogramming. Genome-wide analysis of H3K79me2 distribution revealed that fibroblast-specific genes associated with the epithelial to mesenchymal transition lose H3K79me2 in the initial phases of reprogramming. DOT1L inhibition facilitates the loss of this mark from genes that are fated to be repressed in the pluripotent state. These findings implicate specific chromatin-modifying enzymes as barriers to or facilitators of reprogramming, and demonstrate how modulation of chromatin-modifying enzymes can be exploited to more efficiently generate iPSCs with fewer exogenous transcription factors.
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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.