ArticleMolecular cell2019
Reversible Disruption of Specific Transcription Factor-DNA Interactions Using CRISPR/Cas9.
Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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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
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Systematic Review of Vaccine Strategies Against Tritrichomonas foetus Infection in Cattle: Insights, Challenges, and Prospects.Parasite immunology · 2025Pooled it
- Pooled it
- Article
- Direct Mapping of CDK2 Substrates in Embryonic Stem Cells Uncovers an AP-Site Repair Mechanism via HMCES Phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- The exonic SNP rs11676272-C risk allele mediates diet-induced obesity and reduces enhancer activation.EMBO reports · 2026Article
- YAP-TEAD regulates the super-enhancer network to control early surface ectoderm commitment.Nucleic acids research · 2026Article
- Application of CRISPR-Based Epigenome Editing Tools for Engineering Programmable Embryo Models.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Inhibiting FAT1 Blocks Metabolic Bypass to Enhance Antitumor Efficacy of TCA Cycle Inhibition through Suppressing CPT1A-Dependent Fatty Acid Oxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Blocking the TCA Cycle in Cancer Cells Potentiates CD36+ T-cell-Mediated Antitumor Immunity by Suppressing ER Stress-Associated THBS2 Signaling.Cancer research · 2025Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- Pharmacological restriction of genomic binding sites redirects PU.1 pioneer transcription factor activity.Nature genetics · 2024Article
- Precision epigenetic editing: Technological advances, enduring challenges, and therapeutic applications.Cell chemical biology · 2024Review
- Multicenter integrated analysis of noncoding CRISPRi screens.Nature methods · 2024Article
- Self-organization of embryonic stem cells into a reproducible embryo model through epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- Pioneer and PRDM transcription factors coordinate bivalent epigenetic states to safeguard cell fate.Molecular cell · 2024Article
- Heat shock factor 1 directly regulates transsulfuration pathway to promote prostate cancer proliferation and survival.Communications biology · 2024Article
- Inhibition of OCT4 binding at theFrontiers in oncology · 2024Article
- An intrinsically disordered region controlling condensation of a circadian clock component and rhythmic transcription in the liver.Molecular cell · 2023Article
- SMAD3 promotes expression and activity of the androgen receptor in prostate cancer.Nucleic acids research · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The control of gene expression by transcription factor binding sites frequently determines phenotype. However, it is difficult to determine the function of single transcription factor binding sites within larger transcription networks. Here, we use deactivated Cas9 (dCas9) to disrupt binding to specific sites, a method we term CRISPRd. Since CRISPR guide RNAs are longer than transcription factor binding sites, flanking sequence can be used to target specific sites. Targeting dCas9 to an Oct4 site in the Nanog promoter displaced Oct4 from this site, reduced Nanog expression, and slowed division. In contrast, disrupting the Oct4 binding site adjacent to Pax6 upregulated Pax6 transcription and disrupting Nanog binding its own promoter upregulated its transcription. Thus, we can easily distinguish between activating and repressing binding sites and examine autoregulation. Finally, multiple guide RNA expression allows simultaneous inhibition of multiple binding sites, and conditionally destabilized dCas9 allows rapid reversibility.
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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.