ArticleProceedings of the National Academy of Sciences of the United States of America2016
Reprogramming cell fate with a genome-scale library of artificial transcription factors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 30 citations in OpenAlex.
- Programmable promoter editing for precise control of transgene expression.Nature biotechnology · 2026Article
- Model-guided design of microRNA-based gene circuits supports precise dosage of transgenic cargoes into diverse primary cells.Cell systems · 2025Article
- Development of artificial transcription factors and their applications in cell reprograming, genetic screen, and disease treatment.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Suppression of non-muscle myosin II boosts T cell cytotoxicity against tumors.Science advances · 2024Article
- Systematic discovery of DNA-binding tandem repeat proteins.Nucleic acids research · 2024Article
- Programmable promoter editing for precise control of transgene expression.bioRxiv : the preprint server for biology · 2024Article
- Model-guided design of microRNA-based gene circuits supports precise dosage of transgenic cargoes into diverse primary cells.bioRxiv : the preprint server for biology · 2024Article
- Promising therapeutic aspects in human genetic imprinting disorders.Clinical epigenetics · 2022Review
- Heinz-resistant tomato cultivars exhibit a lignin-based resistance to field dodder (Cuscuta campestris) parasitism.Plant physiology · 2022Article
- Chromatin Alterations in Neurological Disorders and Strategies of (Epi)Genome Rescue.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Optimizing Calcium Detection Methods in Animal Systems: A Sandbox for Synthetic Biology.Biomolecules · 2021Review
- Using Cell Type-Specific Genes to Identify Cell-Type Transitions Between DifferentFrontiers in cell and developmental biology · 2021Article
- Engineering cell fate: Applying synthetic biology to cellular reprogramming.Current opinion in systems biology · 2020Article
- CRISPR-Based Synthetic Transcription Factors In Vivo: The Future of Therapeutic Cellular Programming.Cell systems · 2020Review
- Excluding Oct4 from Yamanaka Cocktail Unleashes the Developmental Potential of iPSCs.Cell stem cell · 2019Article
- NKX3-1 is required for induced pluripotent stem cell reprogramming and can replace OCT4 in mouse and human iPSC induction.Nature cell biology · 2018Article
- Reprogramming cell fate with artificial transcription factors.FEBS letters · 2018Review
- Synthetic transcription elongation factors license transcription across repressive chromatin.Science (New York, N.Y.) · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Artificial transcription factors (ATFs) are precision-tailored molecules designed to bind DNA and regulate transcription in a preprogrammed manner. Libraries of ATFs enable the high-throughput screening of gene networks that trigger cell fate decisions or phenotypic changes. We developed a genome-scale library of ATFs that display an engineered interaction domain (ID) to enable cooperative assembly and synergistic gene expression at targeted sites. We used this ATF library to screen for key regulators of the pluripotency network and discovered three combinations of ATFs capable of inducing pluripotency without exogenous expression of Oct4 (POU domain, class 5, TF 1). Cognate site identification, global transcriptional profiling, and identification of ATF binding sites reveal that the ATFs do not directly target Oct4; instead, they target distinct nodes that converge to stimulate the endogenous pluripotency network. This forward genetic approach enables cell type conversions without a priori knowledge of potential key regulators and reveals unanticipated gene network dynamics that drive cell fate choices.
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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.