DNA Methylation Increase Gene Expression: Mechanisms and Evidence

By Dr. Zubair Khalid, DVM, MS, PhD ·

DNA Methylation Increase Gene Expression: Mechanisms and Evidence

Introduction to DNA Methylation and Gene Expression

What is DNA Methylation?

DNA methylation is a covalent chemical modification in which a methyl group (–CH₃) is transferred to the fifth carbon position of a cytosine base, producing 5-methylcytosine (5mC). In mammals, this reaction is catalyzed by a family of enzymes called DNA methyltransferases (DNMTs): DNMT1 maintains existing methylation patterns during DNA replication, while DNMT3A and DNMT3B establish new methylation marks at previously unmethylated sites. The methyl donor is S-adenosylmethionine (SAM), and the reaction occurs predominantly at cytosine residues followed by guanine—the so-called CpG dinucleotide. Approximately 70–80% of CpG sites in the human genome are methylated, though the distribution is far from uniform.

CpG dinucleotides are underrepresented in the genome overall, but they cluster in regions called CpG islands—stretches of 200 bp to several kilobases with a high GC content and a high observed-to-expected CpG ratio. About 60–70% of human gene promoters are associated with CpG islands. In normal somatic cells, these promoter-associated CpG islands are typically unmethylated, regardless of whether the gene is active or silent. Methylation is more commonly found in intergenic regions, repetitive elements, and the bodies of actively transcribed genes.

The Classic View: Methylation and Silencing

The textbook narrative has long held that DNA methylation is a repressive epigenetic mark. This view is grounded in several well-established observations. First, methylation of promoter CpG islands is strongly associated with transcriptional silencing—a phenomenon frequently exploited by cancer cells to inactivate tumor suppressor genes. Second, methylation of imprinted genes maintains parent-of-origin-specific expression patterns, as described in Imprinting Gene. Third, methylation of transposable elements and repetitive sequences suppresses their mobility, contributing to genomic stability. Fourth, the maintenance of methylation patterns by DNMT1 during cell division provides a mechanism for heritable gene silencing.

The molecular basis for methylation-associated silencing is also well understood. Methylated CpG dinucleotides are recognized by a family of proteins containing a methyl-CpG-binding domain (MBD), including MeCP2, MBD1, MBD2, and MBD3. These proteins recruit co-repressor complexes containing histone deacetylases (HDACs), which remove acetyl groups from histone tails, leading to chromatin compaction. Additionally, methylated DNA can directly interfere with the binding of certain transcription factors whose recognition sequences contain CpG dinucleotides. The combined effect is a condensed chromatin state that is refractory to transcriptional initiation.

However, this canonical view is incomplete. A growing body of evidence demonstrates that DNA methylation can also be associated with increased gene expression, depending on the genomic context. This article examines the mechanisms, experimental evidence, and interpretive nuances of this less-appreciated role of DNA methylation.

Mechanisms by Which DNA Methylation Increases Gene Expression

Inhibition of Repressor Binding

One of the most direct mechanisms by which DNA methylation can increase gene expression is by preventing the binding of transcriptional repressors. Many repressor proteins recognize specific DNA sequences that contain CpG dinucleotides. When these CpG sites become methylated, the repressor can no longer bind, and the gene is released from repression.

A well-characterized example involves the CCCTC-binding factor (CTCF), a zinc-finger protein with diverse roles in chromatin organization. CTCF acts as an insulator that can block enhancer-promoter interactions and establish chromatin domain boundaries. The binding of CTCF to its recognition sequence is highly sensitive to DNA methylation: methylation of CpG sites within the CTCF binding motif abolishes CTCF binding. In the imprinted IGF2-H19 locus, methylation of the differentially methylated region (DMR) on the paternal allele prevents CTCF binding, allowing an enhancer to activate IGF2 expression. On the maternal allele, the DMR is unmethylated, CTCF binds, and the enhancer is insulated from the IGF2 promoter, keeping the gene silent. Here, DNA methylation does not directly activate transcription—it removes a roadblock, and the gene's own enhancers do the rest.

A similar logic applies to the transcriptional repressor REST (RE1-silencing transcription factor), which silences neuronal genes in non-neuronal tissues. REST binds to a conserved 21-bp RE1 motif that contains CpG dinucleotides in some genes. Methylation of these CpG sites can impair REST binding, thereby derepressing target genes. This mechanism illustrates a general principle: when a repressor's binding site overlaps with CpG dinucleotides, methylation can shift the balance from repression toward activation.

Recruitment of Transcriptional Activators

Beyond blocking repressors, DNA methylation can directly recruit proteins that stimulate transcription. The best-studied example is the CXXC finger protein 1 (CFP1), encoded by the CXXC1 gene. CFP1 contains a CXXC domain that specifically binds unmethylated CpG dinucleotides, and it is a component of the SETD1A histone methyltransferase complex, which deposits the activating H3K4me3 mark at promoters. This is a case where unmethylated DNA promotes activation.

However, certain transcription factors preferentially bind methylated DNA. The most prominent example is the family of Krüppel-associated box zinc-finger proteins (KRAB-ZFPs), which generally repress transcription. But other proteins show the opposite behavior. For instance, the transcription factor Kaiso (ZBTB33) binds methylated CpG dinucleotides through its zinc-finger domain and can function as either a repressor or an activator depending on the promoter context. Similarly, the ETS family transcription factor ELK3 has been reported to bind methylated DNA and activate transcription of specific target genes.

Perhaps the most compelling case comes from studies of the C/EBPα (CCAAT/enhancer-binding protein alpha) transcription factor. C/EBPα is a master regulator of adipocyte differentiation and myeloid cell development. Its binding site contains a CpG dinucleotide, and methylation of this site increases C/EBPα binding affinity in vitro. In differentiating adipocytes, methylation at specific C/EBPα binding sites in the PPARγ locus is associated with increased PPARγ expression, a key step in adipogenesis. This demonstrates that methylation can be an active, instructive signal for transcriptional activation, not merely a passive consequence of repressor exclusion.

Chromatin Remodeling and Histone Modifications

DNA methylation does not act in isolation; it is intimately connected to chromatin structure. The traditional view holds that methylation recruits MBD proteins, which in turn recruit HDACs, producing a closed chromatin conformation. However, this is only one possible outcome. Methylated DNA can also recruit proteins that promote an open chromatin state.

The protein UHRF1 (ubiquitin-like with PHD and RING finger domains 1) is a good example of the complexity. UHRF1 binds hemimethylated DNA during replication and recruits DNMT1 to maintain methylation patterns. But UHRF1 also contains a plant homeodomain (PHD) that recognizes H3K9me3, a repressive histone mark. This dual recognition links DNA methylation to repressive chromatin.

In contrast, the methyl-CpG-binding protein MBD3, a component of the nucleosome remodeling and deacetylase (NuRD) complex, has been shown in some contexts to associate with actively transcribed genes. The NuRD complex contains both HDACs and the chromatin remodeling ATPase CHD4, and its net effect on transcription depends on the local balance of histone-modifying enzymes. In embryonic stem cells, MBD3/NuRD occupies promoters of active genes and is required for their proper expression, suggesting that the same methyl-CpG-binding machinery can have context-dependent effects.

Another important player is the histone variant H2A.Z, which is enriched at the promoters of active genes and at CpG islands. H2A.Z deposition is antagonized by DNA methylation: methylated CpG islands exclude H2A.Z, while unmethylated CpG islands recruit it. This creates a feedback loop where DNA methylation status influences nucleosome composition and, consequently, transcriptional activity. In gene bodies, however, methylation and H2A.Z can coexist, and the functional outcome differs from that at promoters.

Evidence from Genomic Studies

Gene Body Methylation and Transcription

Genome-wide methylation profiling has revealed that the relationship between DNA methylation and gene expression is highly position-dependent. While promoter methylation is generally associated with repression, methylation within the transcribed region—the gene body—is positively correlated with gene expression levels. This finding has been replicated across multiple species, including humans, mice, and plants.

Gene body methylation is defined as 5mC within exons and introns downstream of the transcription start site. In highly expressed genes, gene body methylation is typically elevated compared to genes with low or moderate expression. The mechanism is thought to involve transcription-coupled methylation: as RNA polymerase II traverses the gene, it recruits DNMT3B to the transcribed region, which methylates CpG sites in a processive manner. This methylation may serve several functions, including suppressing spurious transcription initiation from cryptic promoters within the gene body, regulating alternative splicing, and stabilizing nucleosome positioning.

The relationship between gene body methylation and splicing is particularly intriguing. Methylated CpG sites within exons can recruit the methyl-CpG-binding protein MeCP2, which in turn slows RNA polymerase II elongation. This kinetic pause provides a window for the spliceosome to recognize weak splice sites, promoting exon inclusion. Conversely, unmethylated exons are associated with faster polymerase elongation and exon skipping. Thus, gene body methylation can increase the expression of specific splice isoforms by modulating co-transcriptional splicing decisions.

It is important to note that gene body methylation is not a prerequisite for transcription—many actively transcribed genes have low gene body methylation. Rather, it appears to be a consequence of transcription that has evolved to serve regulatory functions. The positive correlation between gene body methylation and expression is robust at the population level, but individual genes can deviate from this pattern.

Enhancer Methylation and Activity

Enhancers are regulatory DNA elements that can activate transcription from distal promoters, sometimes over distances of hundreds of kilobases. The relationship between enhancer methylation and activity is complex and context-dependent, as discussed in Gene Promoter vs Enhancer. In general, enhancers that are active in a given cell type tend to have low methylation, while inactive enhancers are hypermethylated. This is consistent with the repressive role of methylation at regulatory elements.

However, there are notable exceptions. Some active enhancers are methylated, and in certain cases, methylation appears to be required for enhancer function. For example, in the developing mouse brain, a subset of active enhancers is methylated at non-CpG sites (CH contexts, where H is A, C, or T). This non-CpG methylation is deposited by DNMT3A and is enriched at enhancers that regulate neuronal genes. The presence of non-CpG methylation distinguishes these enhancers from CpG-methylated inactive enhancers and correlates with active chromatin marks such as H3K27ac.

The functional significance of enhancer methylation is further supported by studies of transcription factor binding. Many transcription factors have CpG-containing binding motifs, and methylation can either enhance or inhibit binding depending on the factor. For instance, the pioneer factor FOXA1 binds to methylated and unmethylated DNA with similar affinity, allowing it to open chromatin at methylated enhancers. In contrast, the binding of factors such as MYF5 and MYOD is inhibited by methylation. The net effect of enhancer methylation on gene expression therefore depends on the specific combination of transcription factors present in a given cell type.

Methods to Study DNA Methylation and Expression

Bisulfite Sequencing

The gold standard for measuring DNA methylation at single-nucleotide resolution is bisulfite conversion followed by sequencing. Treatment of genomic DNA with sodium bisulfite converts unmethylated cytosines to uracil, while methylated cytosines remain unchanged. After PCR amplification, uracils are read as thymines, allowing the methylation status of each CpG site to be inferred from the sequence.

The standard protocol involves the following steps:

  1. Denature genomic DNA (1–2 μg) in 0.3 M NaOH for 15 minutes at 37°C.
  2. Add freshly prepared sodium bisulfite solution (3 M sodium bisulfite, 0.5 mM hydroquinone, pH 5.0) and incubate for 16 hours at 50°C in the dark.
  3. Desalt the DNA using a column-based purification kit.
  4. Desulfonate the DNA by incubation in 0.3 M NaOH for 15 minutes at 37°C.
  5. Precipitate the DNA with ethanol and resuspend in Tris-EDTA buffer.
  6. Perform PCR with primers designed to amplify bisulfite-converted DNA, then sequence the products.

Bisulfite sequencing can be performed on individual loci (targeted bisulfite PCR followed by Sanger sequencing or clonal sequencing) or genome-wide (whole-genome bisulfite sequencing, WGBS). WGBS provides comprehensive coverage but is expensive and requires substantial bioinformatics expertise. Reduced representation bisulfite sequencing (RRBS) enriches for CpG-rich regions using restriction enzymes such as MspI, which cuts at CCGG sites, reducing the sequencing cost while maintaining coverage of most CpG islands and promoters.

Methylated DNA Immunoprecipitation (MeDIP)

MeDIP is an antibody-based approach that enriches for methylated DNA fragments. In this method, genomic DNA is sonicated to fragments of 300–500 bp, denatured, and incubated with a monoclonal antibody specific for 5-methylcytosine. The antibody-DNA complexes are immunoprecipitated using protein A/G beads, and the enriched DNA is then analyzed by quantitative PCR (MeDIP-qPCR), microarray (MeDIP-chip), or high-throughput sequencing (MeDIP-seq).

MeDIP has the advantage of being relatively inexpensive and requiring less DNA than WGBS. However, it does not provide single-nucleotide resolution; instead, it reports the relative enrichment of methylation across a genomic region. The resolution is limited by fragment size, and the antibody's affinity for 5mC can be influenced by the local sequence context and the density of methylated CpGs. MeDIP is therefore best suited for comparing methylation levels between conditions or cell types rather than for absolute quantification.

An alternative enrichment-based method is methyl-CpG-binding domain (MBD) capture, which uses the MBD domain of MeCP2 to pull down methylated DNA. MBD capture has a different bias than MeDIP: it preferentially enriches for regions with high CpG density, whereas MeDIP can detect methylation at low CpG density. Combining both methods can provide complementary views of the methylome.

Integrative Analysis with RNA-seq

To determine whether DNA methylation increases gene expression, it is necessary to correlate methylation data with transcript abundance. RNA-seq is the standard method for quantifying gene expression, and its analysis is covered in detail in Differential Gene Expression Analysis Deseq2 and Differential Gene Expression Dge Analysis. The typical workflow for integrative analysis is:

  1. Generate matched DNA methylation and RNA-seq data from the same biological samples.
  2. Align sequencing reads to the reference genome.
  3. Quantify methylation levels (e.g., percent methylation per CpG site or per genomic region) and gene expression levels (e.g., transcripts per million, TPM).
  4. Correlate methylation at promoters, gene bodies, or enhancers with expression of the associated genes.
  5. Adjust for confounders such as cell-type composition and genetic variation.

A common pitfall in integrative analysis is the direction of causality. A correlation between gene body methylation and expression does not prove that methylation causes increased expression; it may simply reflect the fact that transcription promotes methylation. To address this, researchers use causal inference methods, such as Mendelian randomization, or examine the temporal order of methylation and expression changes in time-course experiments. These approaches are discussed further in Gene Expression Change Over Time.

Context-Dependent Effects of DNA Methylation

Promoter vs. Gene Body Methylation

The most important determinant of whether DNA methylation increases or decreases gene expression is the genomic location of the methylation mark. Promoter methylation, particularly at CpG islands near the transcription start site, is overwhelmingly associated with transcriptional repression. This is because promoter methylation blocks the assembly of the pre-initiation complex, recruits repressive MBD proteins, and promotes a closed chromatin state.

In contrast, gene body methylation is positively correlated with expression. The mechanistic basis for this difference lies in the distinct functions of these regions. Promoters are sites of transcriptional initiation, where the chromatin must be accessible to RNA polymerase and general transcription factors. Gene bodies are sites of transcriptional elongation and co-transcriptional processing, where methylation can regulate splicing and suppress cryptic initiation without interfering with the main transcription machinery.

The transition between these opposing effects is not abrupt. In some genes, methylation at the promoter-proximal region (the first few hundred base pairs downstream of the transcription start site) can have activating effects, while methylation further upstream is repressive. This gradient reflects the differential sensitivity of promoter elements to methylation and the presence of methylation-sensitive transcription factors that bind in the proximal promoter.

Cell-Type Specificity

The effect of DNA methylation on gene expression is also cell-type specific. A methylation mark that activates a gene in one cell type may have no effect or a repressive effect in another. This is because the transcriptional outcome of methylation depends on the repertoire of DNA-binding proteins and chromatin regulators expressed in the cell.

For example, the MAGEA1 gene, which encodes a melanoma-associated antigen, is silenced in most normal tissues but expressed in certain cancers. The promoter of MAGEA1 is unmethylated in expressing cells and methylated in non-expressing cells, consistent with the classic repressive role of promoter methylation. However, in some cancer cell lines, MAGEA1 expression is observed despite partial promoter methylation, suggesting that the activating transcription factors present in these cells can overcome the repressive effect of methylation.

Cell-type specificity also arises from the differential expression of methyl-CpG-binding proteins. Cells that express high levels of MBD2, which recruits repressive complexes, may show stronger methylation-associated silencing than cells with low MBD2. Conversely, cells expressing proteins that bind methylated DNA and activate transcription, such as certain KRAB-ZFP family members, may show methylation-associated activation. The same methylation mark can therefore have opposite effects in different cellular contexts.

Common Misconceptions and Pitfalls

Oversimplifying Methylation as a Silencing Mark

The most common error students make is treating DNA methylation as a binary switch: methylated equals off, unmethylated equals on. This oversimplification fails to account for the position-dependent effects described above. A student who memorizes "methylation silences genes" will be unable to explain why highly expressed genes often have high gene body methylation or why some enhancers are methylated when active.

A more accurate framework is to think of DNA methylation as a context-dependent modulator of transcription. The effect of a methylation mark depends on:

  • The genomic location (promoter, gene body, enhancer, insulator)
  • The CpG density of the region
  • The specific transcription factors and chromatin regulators present in the cell
  • The developmental stage and environmental conditions

When answering exam questions, always specify the genomic context. A statement like "promoter CpG island methylation is associated with transcriptional repression" is defensible; "DNA methylation represses transcription" is not.

Correlation vs. Causation

A second pitfall is confusing correlation with causation. When a genomic study finds that gene body methylation correlates with increased expression, it is tempting to conclude that methylation causes the increase. However, the causal relationship may be reversed: transcription may cause methylation. RNA polymerase II can recruit DNMT3B to gene bodies, and the act of transcription may promote the maintenance of methylation at these sites.

To distinguish causation from correlation, consider the following criteria:

  • Temporal precedence: Does methylation appear before the change in expression, or after?
  • Dose-response: Does the magnitude of methylation correlate with the magnitude of expression change?
  • Manipulation: Does experimentally altering methylation (e.g., by DNMT inhibitors or targeted demethylation) change expression in the predicted direction?
  • Mechanistic plausibility: Is there a known molecular mechanism by which the methylation mark could affect transcription?

In many cases, the relationship is bidirectional: methylation can influence transcription, and transcription can influence methylation. This feedback loop complicates interpretation and requires careful experimental design to disentangle.

Practical Summary and Study Tips

Key Takeaways

  • DNA methylation is the covalent addition of a methyl group to cytosine, catalyzed by DNMT enzymes, and occurs predominantly at CpG dinucleotides.
  • The canonical role of DNA methylation is transcriptional repression, mediated by MBD proteins and histone deacetylases.
  • DNA methylation can increase gene expression by blocking repressor binding, recruiting activating transcription factors, and modulating chromatin structure.
  • Gene body methylation is positively correlated with gene expression and may regulate splicing and suppress cryptic transcription.
  • Enhancer methylation has context-dependent effects; some active enhancers are methylated, particularly at non-CpG sites in neurons.
  • The effect of DNA methylation depends on genomic location, cell type, and developmental stage.
  • Bisulfite sequencing and MeDIP are the primary methods for measuring methylation; integrative analysis with RNA-seq is essential for linking methylation to expression.

Exam Preparation Tips

  1. Learn the exceptions: The classic silencing model is the baseline, but you must know the exceptions to score well. Focus on gene body methylation and the CTCF/insulator example.
  1. Draw the mechanisms: Practice drawing diagrams of how methylation blocks repressor binding (CTCF at IGF2-H19) and how gene body methylation affects splicing. Visual memory will help you recall these pathways in exams.
  1. Use the location framework: When asked about the effect of methylation on a gene, always ask: Where is the methylation? Promoter, gene body, or enhancer? This will guide your answer.
  1. Know the methods: Be able to explain the principle of bisulfite conversion (unmethylated C → U → T) and why it allows methylation detection. Understand the difference between WGBS and MeDIP.
  1. Connect to related topics: Understand how methylation relates to Gene Silencing and how it differs from other regulatory mechanisms. The ability to compare and contrast will demonstrate deeper understanding.
  1. Practice with real data: If you have access to methylation and expression data, try correlating gene body methylation with expression levels. This will reinforce the concepts and prepare you for data interpretation questions.

Frequently Asked Questions

Can DNA methylation increase gene expression?

Yes. DNA methylation can increase gene expression through several mechanisms, including blocking the binding of transcriptional repressors, recruiting transcriptional activators, and modulating chromatin structure. The most well-documented example is gene body methylation, which is positively correlated with gene expression levels. Additionally, methylation at specific enhancers and insulator elements can release genes from repression, indirectly increasing their expression.

Does DNA methylation always repress gene expression?

No. While promoter CpG island methylation is typically associated with repression, methylation in other genomic contexts can have neutral or activating effects. Gene body methylation is positively correlated with expression, and some transcription factors preferentially bind methylated DNA to activate transcription. The effect of methylation depends on its genomic location, the local chromatin context, and the specific proteins present in the cell.

How can DNA methylation increase transcription?

DNA methylation can increase transcription by: (1) preventing repressor proteins such as CTCF from binding to their recognition sites, thereby removing a block on enhancer-promoter communication; (2) recruiting activating transcription factors that specifically recognize methylated CpG dinucleotides; and (3) promoting chromatin states that are permissive for transcription, for example by influencing histone variant deposition or nucleosome positioning. In gene bodies, methylation can also increase expression of specific splice isoforms by modulating RNA polymerase II elongation.

What is gene body methylation?

Gene body methylation refers to 5-methylcytosine within the transcribed region of a gene, downstream of the transcription start site. It is enriched in exons and introns of actively transcribed genes and is positively correlated with expression levels. Gene body methylation is thought to suppress spurious transcription initiation from cryptic promoters, regulate alternative splicing, and stabilize nucleosome positioning. It is deposited co-transcriptionally by DNMT3B recruited by RNA polymerase II.

What techniques are used to study DNA methylation?

The main techniques are bisulfite sequencing (including whole-genome bisulfite sequencing and reduced representation bisulfite sequencing), which provides single-nucleotide resolution; methylated DNA immunoprecipitation (MeDIP), which enriches methylated fragments using an anti-5mC antibody; and methyl-CpG-binding domain (MBD) capture, which uses the MBD domain of MeCP2. These methods are often combined with RNA-seq to correlate methylation with gene expression.

Why is DNA methylation sometimes associated with active genes?

DNA methylation is associated with active genes primarily because of gene body methylation, which accumulates as a consequence of transcription. RNA polymerase II recruits DNMT3B during elongation, leading to methylation of the transcribed region. This methylation can then regulate splicing and suppress cryptic transcription initiation. Additionally, some enhancers and transcription factor binding sites are methylated when active, and methylation can block repressor binding at insulator elements, allowing enhancers to activate their target genes.

Is the effect of DNA methylation on gene expression universal?

No. The effect of DNA methylation on gene expression is highly context-dependent. It varies by genomic location (promoter vs. gene body vs. enhancer), CpG density, cell type, developmental stage, and the specific transcription factors and chromatin regulators expressed in the cell. A methylation mark that activates a gene in one context may repress it in another. Therefore, the effect of methylation must be evaluated on a case-by-case basis, considering the full regulatory environment of the gene.

Key Takeaways

  • DNA methylation is a covalent modification of cytosine at CpG dinucleotides, catalyzed by DNMT1 (maintenance) and DNMT3A/3B (de novo).
  • The canonical role of promoter CpG island methylation is transcriptional repression, mediated by MBD proteins and HDAC recruitment.
  • DNA methylation can increase gene expression by blocking repressor binding (e.g., CTCF at IGF2-H19), recruiting activating factors (e.g., C/EBPα), and modulating chromatin structure.
  • Gene body methylation positively correlates with gene expression and regulates splicing and cryptic transcription suppression.
  • Enhancer methylation is context-dependent; some active enhancers are methylated, particularly at non-CpG sites in neurons.
  • The effect of methylation depends on genomic location, cell type, and developmental stage—there is no universal rule.
  • Bisulfite sequencing (WGBS, RRBS) and MeDIP are the primary methods for methylation analysis; integration with RNA-seq is essential for functional interpretation.

Further Reading

  • Soci UPR et al. Exercise Training and Epigenetic Regulation: Multilevel Modification and Regulation of Gene Expression. Advances in experimental medicine and biology. 2017. PubMed 29098627
  • Joshi SR et al. Hypoxic activation of glucose-6-phosphate dehydrogenase controls the expression of genes involved in the pathogenesis of pulmonary hypertension through the regulation of DNA methylation. American journal of physiology. Lung cellular and molecular physiology. 2020. PubMed 32159369
  • Zou L et al. Gene body demethylation increases expression and is associated with self-pruning during grape genome duplication. Horticulture research. 2020. PubMed 32528696
  • Chen H et al. Chronic inorganic arsenic exposure induces hepatic global and individual gene hypomethylation: implications for arsenic hepatocarcinogenesis. Carcinogenesis. 2004. PubMed 15073043
  • Górska A et al. Genome-Wide DNA Methylation and Gene Expression in Patients with Indolent Systemic Mastocytosis. International journal of molecular sciences. 2023. PubMed 37762215
  • Zhou M et al. Age-related gene expression and DNA methylation changes in rhesus macaque. Genomics. 2020. PubMed 32927008

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