ArticleNucleic acids research2019
Antagonistic and synergistic epigenetic modulation using orthologous CRISPR/dCas9-based modular system.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Large glycomics datasets as a tool to understand the function of glycans.Nature chemical biology · 2026Review
- B cell mechanisms underlie IgG glycan alterations in obesity.Glycobiology · 2026Article
- DNA Methylation as a Programmable Information Layer: From Molecular Marks to Disease State Engineering.International journal of molecular sciences · 2026Review
- CRISPR/Cas‑based epigenome editing for osteogenic lineage commitment.Cell and tissue research · 2026Review
- Combinatorial and Inducible CRISPRa/i Enables Canalized hiPSC Forward Programming and Iterative RefinementbioRxiv : the preprint server for biology · 2026Article
- Target therapeutic exploitation of engineered exosome-mediated delivery of ncRNAs in cancer.Cancer gene therapy · 2026Review
- The Future of Epigenetics: Emerging Technologies and Clinical Applications.ACS pharmacology & translational science · 2026Review
- Comprehensive profiling of CRISPR/dCas9 epigenome editors indicates a complex link between on and off target effects.Genome biology · 2026Article
- Article
- Cell-type- and locus-specific epigenetic editing of memory expression.Nature genetics · 2025Article
- Bidirectional epigenetic editing reveals hierarchies in gene regulation.Nature biotechnology · 2025Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- Integration of CRISPR/dCas9-Based methylation editing with guide positioning sequencing identifies dynamic changes of mrDEGs in breast cancer progression.Cellular and molecular life sciences : CMLS · 2025Article
- Harnessing the evolving CRISPR/Cas9 for precision oncology.Journal of translational medicine · 2024Review
- A genetic-epigenetic interplay at 1q21.1 locus underlies CHD1L-mediated vulnerability to primary progressive multiple sclerosis.Nature communications · 2024Article
- Recent advances in N-glycan biomarker discovery among human diseases.Acta biochimica et biophysica Sinica · 2024Review
- Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- Targeted DNA Methylation Editing Using an All-in-One System Establishes Paradoxical Activation ofCancers · 2024Article
- TET (Ten-eleven translocation) family proteins: structure, biological functions and applications.Signal transduction and targeted therapy · 2023Review
- The Design and Application of DNA-Editing Enzymes as Base Editors.Annual review of biochemistry · 2023Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Establishing causal relationship between epigenetic marks and gene transcription requires molecular tools, which can precisely modify specific genomic regions. Here, we present a modular and extensible CRISPR/dCas9-based toolbox for epigenetic editing and direct gene regulation. It features a system for expression of orthogonal dCas9 proteins fused to various effector domains and includes a multi-gRNA system for simultaneous targeting dCas9 orthologs to up to six loci. The C- and N-terminal dCas9 fusions with DNMT3A and TET1 catalytic domains were thoroughly characterized. We demonstrated simultaneous use of the DNMT3A-dSpCas9 and TET1-dSaCas9 fusions within the same cells and showed that imposed cytosine hyper- and hypo-methylation altered level of gene transcription if targeted CpG sites were functionally relevant. Dual epigenetic manipulation of the HNF1A and MGAT3 genes, involved in protein N-glycosylation, resulted in change of the glycan phenotype in BG1 cells. Furthermore, simultaneous targeting of the TET1-dSaCas9 and VPR-dSpCas9 fusions to the HNF1A regulatory region revealed strong and persistent synergistic effect on gene transcription, up to 30 days following cell transfection, suggesting involvement of epigenetic mechanisms in maintenance of the reactivated state. Also, modulation of dCas9 expression effectively reduced off-target effects while maintaining the desired effects on target regions.
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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.