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Trusted by Leading Research & Pharma Institutions

Epigenome Editing Services

Precisely modulate gene expression by rewriting chemical marks on DNA and histones without altering the underlying sequence. Our CRISPR-dCas9 platform enables surgical accuracy in epigenetic regulation for groundbreaking research and therapeutic development.

No DNA Breaks
Heritable Modifications
High Specificity
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Trusted by leading research and pharmaceutical institutions

MIT
Pfizer
Stanford
Novartis
Johns Hopkins
Roche

Why Choose Our Epigenome Editing

CRISPR-dCas9 precision targeting
Multiple effector options (DNMT, TET, p300, KRAB)
Works in non-dividing cells
Heritable epigenetic modifications

DNA Methylation Editing

Targeted CpG methylation/demethylation for gene silencing

Histone Modification

H3K27ac and other histone marks for activation

CRISPRi/CRISPRa

Reversible gene regulation without permanent changes

Genomic Safety
No DSBs
Service Overview

Precision Gene Regulation Without Altering the DNA Sequence

Our epigenome editing platform enables targeted modulation of gene expression by rewriting chemical marks on DNA or histones, offering unprecedented precision for basic research and therapeutic development.

CRISPR-dCas9 Platform

Our advanced CRISPR-dCas9 platform utilizes catalytically inactive Cas9 fused to various epigenetic effector domains. This approach allows precise targeting of specific genomic loci without introducing double-strand breaks, ensuring superior safety and precision.

  • dCas9-DNMT3A for targeted methylation
  • dCas9-TET1 for demethylation
  • dCas9-p300 for histone acetylation
  • dCas9-KRAB for transcriptional repression

Safety & Precision

Unlike traditional CRISPR editing that introduces DNA breaks, epigenome editing modifies gene expression without altering the underlying DNA sequence. This approach avoids mutations, translocations, and p53-mediated toxicity.

  • No double-strand breaks
  • Works in non-dividing cells
  • Reduced off-target effects
  • Reversible modifications possible

Heritable Modifications

DNA methylation changes can be stably inherited through cell divisions for lasting phenotypic changes.

Multiplex Capability

Target multiple promoters or enhancers simultaneously to regulate entire metabolic networks.

RNP Delivery

High-efficiency ribonucleoprotein delivery minimizes cytotoxicity in primary cells.

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Technology Platform

Advanced Epigenome Editing Tools

Our comprehensive platform offers multiple effector options to meet diverse research needs.

DNA Methylation Editors

Targeted DNA methylation using dCas9 fused to DNMT3A catalytic domain for stable gene silencing.

dCas9-DNMT3A dCas9-DNMT3L

DNA Demethylation Editors

Targeted demethylation using TET1 dioxygenase to reactivate silenced genes.

dCas9-TET1 dCas9-TETv4

Histone Modification Editors

Epigenetic writers and erasers for precise histone mark manipulation.

dCas9-p300 dCas9-KRAB dCas9-LSD1

CRISPRi/CRISPRa Systems

CRISPRi Transcriptional silencing via KRAB recruitment
CRISPRa Transcriptional activation via VPR/p300
CRISPRoff Heritable gene silencing system

Delivery Methods

RNP Ribonucleoprotein for minimal toxicity
Lentivirus Stable integration for long-term studies
AAV In vivo delivery compatibility
Specifications

Service Specifications

Comprehensive specifications to meet your research requirements.

Parameter DNA Methylation DNA Demethylation Histone Editing
Effector Proteins dCas9-DNMT3A, dCas9-DNMT3L dCas9-TET1, dCas9-TETv4 dCas9-p300, dCas9-KRAB, dCas9-LSD1
Modification Type CpG methylation 5mC demethylation H3K27ac, H3K9me3, H3K4me
Modification Range 300-500 bp 150-200 bp Target-specific
Heritability Stable, heritable Variable Often transient
Reversibility Can be reversed by TET Permanent once established Generally reversible
Cell Types Dividing and non-dividing Dividing and non-dividing All cell types
Workflow

Streamlined Process from Design to Delivery

Our proven workflow ensures quality and efficiency at every stage.

1

Target Identification

Bioinformatic analysis of chromatin accessibility (ATAC-seq/ChIP-seq)

2

System Design

Select optimal dCas9 effector fusion based on desired outcome

3

gRNA Design

Custom gRNA library design for high-precision targeting

4

Delivery & Validation

RNP/mRNA/viral delivery with real-time monitoring

5

Characterization

Bisulfite-seq/ChIP-qPCR and transcriptional analysis

Applications

Diverse Research Applications

Our epigenome editing services support a broad spectrum of research areas.

T-Cell Engineering for Cancer Therapy

Enhance immune cell function by modulating checkpoint genes through epigenome editing. Silence immune checkpoint genes like PD-1 via repressive histone marks to enhance anti-tumor performance without permanent DNA alteration.

  • Programmable epigenetic repression of checkpoint genes
  • RNP delivery minimizes cytotoxicity in primary T-cells
  • Reversible modifications for controlled immune response

Key Advantages

No DNA alterations in therapeutic cells
Transient delivery reduces off-target risks
Preserve genomic integrity for clinical applications
Testimonials

What Researchers Say

Trusted by scientists worldwide for epigenome editing research.

"The epigenome editing platform allowed us to precisely study the role of DNA methylation in gene regulation without introducing DNA breaks. The results were highly reproducible across multiple cell types."

Senior Scientist

Biotechnology Company

"Using dCas9-TET1 for targeted demethylation, we successfully reactivated silenced tumor suppressor genes in our cancer model. The precision and efficiency exceeded our expectations."

Research Director

Pharmaceutical Research Institution

"The service's flexibility in designing custom gRNA libraries for our imprinting disease research was invaluable. The technical support team provided excellent consultation throughout."

Principal Investigator

Academic Research Institution

Scientific Literature

Supporting Publications

Our epigenome editing platform is backed by peer-reviewed research.

286 Citations

CRISPR/Cas9 Epigenome Editing Potential for Rare Imprinting Diseases: A Review

Linn Amanda Syding, Petr Nickl, Petr Kasparek, Radislav Sedlacek | Cells (2020)

View DOI
124 Citations

CRISPR/dCas9 DNA Methylation Editing is Heritable During Human Hematopoiesis and Shapes Immune Progeny

Saunderson E.A, Encabo H.H, Devis J, et al. | PNAS (2023)

View DOI
156 Citations

Epigenome Engineering: New Technologies for Precision Medicine

Agustin Sgro, Pilar Blancafort | Nucleic Acids Research (2020)

View DOI
89 Citations

Toward the Development of Epigenome Editing-Based Therapeutics: Potentials and Challenges

Jun Ueda, Taiga Yamazaki, Hiroshi Funakoshi | IJMS (2023)

View DOI
87 Citations

CRISPR/dCas9 Tools: Epigenetic Mechanism and Application in Gene Transcriptional Regulation

Ruijie Cai, Runyu Lv, Xin'e Shi, Gongshe Yang, Jianjun Jin | IJMS (2023)

View DOI
FAQ

Frequently Asked Questions

Find answers to common questions about epigenome editing services.

Is epigenome editing permanent?

It depends on the modification type. Histone modifications are often transient, while DNA methylation via dCas9-DNMT can lead to stable, heritable gene silencing across cell divisions. DNA demethylation using dCas9-TET1 can permanently remove methylation marks once established.

Can you target distal enhancers far from the gene?

Absolutely. One of the greatest strengths of epigenome editing is targeting distal enhancers and insulators to study the "dark matter" of the genome and its role in long-range gene regulation. This capability is essential for understanding complex regulatory networks.

How do you confirm epigenetic changes were successful?

We use specialized assays including Methylation-Specific PCR, Bisulfite Sequencing, and ChIP-qPCR to verify the addition or removal of chemical marks at the target site. RNA-seq can confirm downstream transcriptional changes.

Does this technology work in non-dividing cells?

Yes. Since epigenome editing does not rely on HDR, it is highly effective in post-mitotic cells such as primary neurons, cardiomyocytes, and resting immune cells. This makes it ideal for studying differentiated cells and hard-to-transfect primary tissues.

What delivery methods are available?

We offer multiple delivery options: RNP complexes for minimal toxicity, lentiviral vectors for stable integration, AAV for in vivo applications, and mRNA for transient expression. The optimal method depends on your cell type and experimental goals.

What are the modification ranges for different effectors?

DNA methylation editors typically affect 300-500 bp regions, while demethylation editors (TET1) work within 150-200 bp downstream of the PAM site. Histone editors provide target-specific modifications without defined ranges. These can be tailored based on your experimental requirements.

Still have questions? Our technical team is here to help.

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