ArticleNature communications2023
Conserved transcription factors promote cell fate stability and restrict reprogramming potential in differentiated cells.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Bridging Organ-on-a-Chip and Omics: A Multi-Dimensional Frontier in Biomedical Research.Biotechnology and bioengineering · 2026Review
- The SynMuvA lin-15A licenses natural transdifferentiation by antagonizing identity safeguarding mechanisms.PLoS genetics · 2026Article
- Multi-omics technologies: Novel tools and methods for assessing nerve injury and regeneration.Neural regeneration research · 2026Article
- Sulfotransferase signaling sustains fibroblast identity and antagonizes therapeutic cardiac reprogramming.Nature communications · 2026Article
- Combinatorial and Inducible CRISPRa/i Enables Canalized hiPSC Forward Programming and Iterative RefinementbioRxiv : the preprint server for biology · 2026Article
- MCVAE-based multi-omic anomaly detection in Fragile X Syndrome.NAR molecular medicine · 2026Article
- Review
- Deep Neural Networks Based on Sp7 Protein Sequence Prediction in Peri-Implant Bone Formation.International journal of dentistry · 2025Article
- Single-cell multi-modal integrative analyses highlight functional dynamic gene regulatory networks directing human cardiac development.Cell genomics · 2024Article
- Cell-fate conversion of intestinal cells in adult Drosophila midgut by depleting a single transcription factor.Nature communications · 2024Article
- The combination of decitabine with multi-omics confirms the regulatory pattern of the correlation between DNA methylation of the CACNA1C gene and atrial fibrillation.Frontiers in pharmacology · 2024Article
- Programming human cell fate: overcoming challenges and unlocking potential through technological breakthroughs.Development (Cambridge, England) · 2023Article
- Can we stop one heart from breaking: triumphs and challenges in cardiac reprogramming.Current opinion in genetics & development · 2023Review
- Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Defining the mechanisms safeguarding cell fate identity in differentiated cells is crucial to improve 1) - our understanding of how differentiation is maintained in healthy tissues or altered in a disease state, and 2) - our ability to use cell fate reprogramming for regenerative purposes. Here, using a genome-wide transcription factor screen followed by validation steps in a variety of reprogramming assays (cardiac, neural and iPSC in fibroblasts and endothelial cells), we identified a set of four transcription factors (ATF7IP, JUNB, SP7, and ZNF207 [AJSZ]) that robustly opposes cell fate reprogramming in both lineage and cell type independent manners. Mechanistically, our integrated multi-omics approach (ChIP, ATAC and RNA-seq) revealed that AJSZ oppose cell fate reprogramming by 1) - maintaining chromatin enriched for reprogramming TF motifs in a closed state and 2) - downregulating genes required for reprogramming. Finally, KD of AJSZ in combination with MGT overexpression, significantly reduced scar size and improved heart function by 50%, as compared to MGT alone post-myocardial infarction. Collectively, our study suggests that inhibition of barrier to reprogramming mechanisms represents a promising therapeutic avenue to improve adult organ function post-injury.
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Registered trials
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