Epigenetics最新文献

{"title":"The role of R-loops-mediated epigenetic regulation in genome stability maintenance and disease pathogenesis: a systematic review.","authors":"Zi Hao Jiang, Di Feng Wang, Rui Shao, Xing Sheng Wang, Zi Ren Tang","doi":"10.1080/15592294.2026.2653959","DOIUrl":"10.1080/15592294.2026.2653959","url":null,"abstract":"<p><p>This systematic review synthesizes current evidence linking R-loops - associated processes with epigenetic regulation, genome stability, and human disease, integrating findings across DNA/RNA/protein modifications and 3D genome organization, and highlighting key mechanistic and technical gaps relevant to future studies, including longer-term translational exploration. Following PRISMA guidelines (Registration No.: INPLASY202560055), PubMed and ScienceDirect databases were searched through 18 January 2026. Two independent reviewers conducted blinded screening via the Rayyan platform. From 1290 initial articles, 71 studies met inclusion criteria. Methodological rigour was assessed using a modified SYRCLE risk-of-bias tool. Thematic synthesis identifies R-loops as recurrent intermediates linking transcription, chromatin regulation, and genome maintenance; feedback-like relationships are reported in selected systems. They spatially impede DNMTs to sustain promoter hypomethylation while recruiting TET enzymes for demethylation, and RNA modifications (e.g. m5C/m6A) may tune hybrid stability and, in some contexts, influence effector recruitment. R-loops facilitate the recruitment of histone-modifying complexes (PRC1/PRC2, G9a/GLP), thereby influencing chromatin landscapes and 3D genome architecture - including associations with TAD boundary insulation and with LLPS-related repair compartments in specific contexts. Dysregulation of R-loop homeostasis links to disease-related epigenetic alterations and genome instability with distinct disease-, locus- and cell-state specificity, and its context-dependent roles in diverse disorders involve transcriptional silencing, DNA damage, replication-transcription conflicts, repair pathways, chromatin regulation and mitochondrial genome maintenance. Integrating DRIP-seq with epigenomic profiling and functional tests supports mapping of context-specific relationships.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2653959"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetics in cardiovascular health, pathology, and development.","authors":"Marta W Szulik, Luis Hortells, Manuel Rosa-Garrido","doi":"10.1080/15592294.2026.2722863","DOIUrl":"10.1080/15592294.2026.2722863","url":null,"abstract":"","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2722863"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of a digital PCR assay targeting plasma <i>FAR1</i> methylation for early detection of hepatocellular carcinoma.","authors":"Sun Jae Park, Yun Young Lee, Yong-Kyu Chung, Bo-Hyun Jung, Joon An, Jinil Han, Youngho Moon, Hee-Jung Wang","doi":"10.1080/15592294.2026.2653956","DOIUrl":"10.1080/15592294.2026.2653956","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, yet current surveillance with alpha-fetoprotein (AFP) and ultrasound (US) lacks sufficient accuracy, particularly for early-stage disease. This study aimed to develop and clinically validate a blood-based digital PCR (dPCR) assay targeting novel methylation biomarkers for HCC detection. Genome-wide methylation profiles from HCC, normal, and other cancer types were analysed to identify candidates, which were then screened and verified in cancer cell lines, primary tumour tissues, and plasma specimens. A total of 186 plasma samples were evaluated, including 66 healthy controls, 60 patients with chronic liver disease (CLD) without HCC, and 60 patients with HCC. <i>FAR1</i> methylation emerged as an HCC-specific biomarker, showing significantly higher levels in liver cancer cell lines and HCC tumour tissues compared with controls. A dPCR assay targeting <i>FAR1</i> achieved 70.0% sensitivity (42/60; 95% CI, 56.8%-81.2%) and 96.8% specificity (122/126; 95% CI, 92.1-99.1%), with an area under the curve (AUC) of 0.90 (95% CI, 0.85-0.96). Combining <i>FAR1</i> with AFP improved sensitivity to 88.3% (53/60; 95% CI, 77.4%-95.2%) while maintaining 96.8% specificity. Notably, early-stage HCC (Barcelona Clinic Liver Cancer [BCLC] stage 0-A) was detected with 85.4% sensitivity (35/41; 95% CI, 77.4%-94.4%). This blood-based dPCR assay demonstrated high diagnostic performance, underscoring its potential as a noninvasive tool to enhance early detection and clinical management of HCC in high-risk populations.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2653956"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics analysis reveals new pathogenic methylation sites, genes, and potential regulatory pathways in essential hypertension.","authors":"Xinmeng Hu, Huizhen Jin, Xiaoyang Li, Zhuoshuai Liang, Jikang Shi, Hongrui Zhang, Jiahui Zhao, Yong Li, Yunkai Liu, Yi Cheng, Yawen Liu","doi":"10.1080/15592294.2026.2653955","DOIUrl":"10.1080/15592294.2026.2653955","url":null,"abstract":"<p><p>The complex pathophysiology of essential hypertension (EH) continues to pose challenges to blood control. This study investigated the association of blood DNA methylation and gene expression with EH in blood and arterial tissues to identify potential pathogenic methylation sites, genes, and mechanisms. We identified 767 methylation sites, 159 blood genes, and 111 arterial genes associated with EH. Among these, 41 genes were consistently associated with EH in the same direction in both blood and arterial tissues. Of these, eight genes (<i>FDFT1</i>, <i>FES</i>, <i>GNL3</i>, <i>NME6</i>, <i>SLC22A5</i>, <i>UBA7</i>, <i>ULK3</i>, and <i>ZNF589</i>) were annotated from the EH-relevant DNA methylation sites. Drug target analysis identified 64 compounds targeting FDFT1, FES, ULK3, and SLC22A5. Integration of summary data-based mendelian randomization (SMR) results revealed 72 and 79 significant DNA methylation-related, gene-proximal regulatory pathways associated with EH in single blood tissue and cross-tissue analyses, respectively. Notably, methylation sites of the <i>FES</i> significantly influenced changes in <i>FES</i> expression in both blood (cg03209642: b_meSMR = -2.199; cg05211768: b_meSMR = -1.613) and arterial tissue (cg06330618: b_meSMR = -0.572), influencing the risk of EH (<i>FES</i> in blood: b_eSMR = -0.013; arterial tissues: b_eSMR = -0.029). The eight methylated genes are associated with the risk of EH in both blood and arterial tissue. <i>NME6</i>, <i>SLC22A5</i>, <i>GNL3</i> and <i>UBA7</i> have been found to be associated with EH. The methylation-mediated regulation of <i>FES</i> may represent a potential new pathway in the blood and arterial tissues. These findings offer valuable insights for the development of EH biomarkers and therapeutic strategies.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2653955"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of breast DNA methylation-based measures of biological ageing with obesity-related breast cancer risk markers.","authors":"Amarnath Singh, Joseph P McElroy, Daniel Y Weng, Sarah A Reisinger, Jo L Freudenheim, Peter G Shields, Min-Ae Song","doi":"10.1080/15592294.2026.2632400","DOIUrl":"10.1080/15592294.2026.2632400","url":null,"abstract":"<p><p>Advancing age and deregulated obesity are well-established risk factors for breast cancer risk. While epigenetic ageing, a measure of biological ageing, has been linked to breast cancer risk, prior studies have mainly focused on blood-based measures. We aimed to study well-established epigenetic age estimates in normal breast tissue in relation to obesity-related metabolic markers. We analysed breast tissue from 91 cancer-free women, using DNA methylation age (mAge) clocks, including first-generation clocks (Hannum, Horvath), mortality-related clocks (Grim, Pheno), and methylation-based telomere length (DNAmTL). Pearson correlations assessed relationships among the clocks. Linear regression was used to associate mAge clocks with obesity-related blood markers (leptin, adiponectin, IGF-1, IGFBP-3), adjusting for chronological age, race, body mass index (BMI), and smoking, applying a false discovery rate threshold of 0.1. We explored effect modification by menopausal status using interaction terms. In the normal breast tissue, the strongest correlation of mAge estimates was observed between Horvath-mAge and Grim-mAge (r = 0.85). BMI was positively associated with all mAge estimates except Pheno-mAge. Older Grim-mAge and longer DNAmTL were associated with higher levels of adiponectin, IGF-1, and IGFBP-3, while older Horvath-mAge was associated only with IGF-1. Associations of DNAmTL with IGF-1 and adiponectin differed statistically by menopausal status. Epigenetic age in breast tissue, particularly Grim and DNAmTL, is associated with obesity-related metabolic markers, independent of chronological age, BMI, and smoking. Although limited by a moderate sample size, our findings indicate a potential biological pathway linking mAge-related metabolic dysregulation that may provide insight into breast cancer risk.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2632400"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide DNA methylation profiles and ribosomal DNA copy number at birth.","authors":"Kathrin Barth, Rossella Alfano, Michelle Plusquin, Congrong Wang, Tim S Nawrot, Dries S Martens","doi":"10.1080/15592294.2026.2633818","DOIUrl":"10.1080/15592294.2026.2633818","url":null,"abstract":"<p><p>Ribosomal DNA copy number (rDNAcn) and DNA methylation are important modulators of the human genome, both studied in relation to overall cellular function, biological ageing, and disease development. Despite the overlapping roles, their relationship remains poorly understood, especially in the early stages of life, characterized by rapid growth and high cellular demands. Even though previous studies have associated rDNA methylation with cancer and ageing, no study to date has examined the interplay between rDNAcn and whole-genome DNA methylation. In an epigenome-wide association study of 45S rDNAcn variation in 194 newborns, we show strong positive associations between rDNAcn and single DNA methylated CpGs, measured with the Illumina EPIC array. Out of the 122 Bonferroni-significant CpGs, 63.5% were also Bonferroni-significant in a replication cohort of 167 newborns, in which a second EWAS was conducted using DNA methylation data from the Illumina 450K array. The identified CpGs were dispersed over the autosomes and were not functionally related to the rDNA-forming nucleolar-associated domains. The top CpGs were annotated to genes (<i>GFI1, USP46</i>, <i>ABHD14B</i>, <i>CHL1</i>, <i>CGREF1</i>) that are functionally linked to cancer and cellular proliferation. In downstream analyses, the 122 rDNAcn-related CpGs revealed 31 differentially methylated regions and 253 nominally significant correlations with cord blood gene transcripts in an eQTM analysis. Pathway enrichment analyses showed an overrepresentation of the following pathways: 'RNA Polymerase III transcription' (R-HSA-76071, R-HSA-76046, R-HSA-74158, R-HSA-749476, R-HSA-73780, R-HSA-73980, R-HSA-76066, R-HSA-76061, hsa03020), 'cytosolic sensors of pathogen-associated DNA' (R-HSA-1834949), 'RNA polymerase II transcribes snRNA genes' (R-HSA-6807505), and 'translation initiation' (R-HSA-72613, R-HSA-72737). Our findings reveal a close link between rDNAcn variation and DNA methylation in early life. Disruptions in this interplay may influence cellular functions critical for early development, potentially shaping health and disease trajectories later in life.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2633818"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12959191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding osteosarcoma pathogenesis: the pivotal influence of m⁶A modification.","authors":"Chaomei Huang, Zhongyu Han, Junyan Su, Meiqi Zhang, Yumeng Lin, Haibei He, Yu Tang, Peng Guo, Yi Wang, Haoran Chen","doi":"10.1080/15592294.2026.2705608","DOIUrl":"10.1080/15592294.2026.2705608","url":null,"abstract":"<p><p>Osteosarcoma (OS) is the predominant primary malignant bone tumor in children and adolescents. Current treatments mainly include surgical resection combined with chemotherapy, but they still cannot effectively control tumor metastasis and recurrence, and may pose a risk of long-term complications. N6-methyladenosine (m⁶A) is the most widespread internal modification. It orchestrates various biological and disease-related events via the reversible m⁶A machinery comprising writers, erasers and readers. As a key epigenetic regulatory mechanism, m⁶A modification opens new avenues for deeper exploration of OS mechanisms and for developing new therapeutic targets and biomarkers. In this manuscript, we systematically explore the critical roles of m⁶A in OS cell proliferation, metastasis, metabolic reprogramming, programmed cell death, and tumor microenvironment regulation. Our aim is to provide a robust theoretical framework to underpin future basic studies and clinical applications in this field.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2705608"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing of optogenetic and chemogenetic transgenes in human iPSCs involves promoter methylation and methylation-independent mechanisms.","authors":"Yiwen Wang, Yanyan Li, Jingzhen Li, Meng Li, Xuecheng Qiu","doi":"10.1080/15592294.2025.2606983","DOIUrl":"10.1080/15592294.2025.2606983","url":null,"abstract":"<p><p>The transplantation of neural progenitor cells derived from induced pluripotent stem cells (iPSCs) has therapeutic potential for the treatment of neurological diseases. However, the functional integration of transplanted iPSC-derived neurons into host neural networks remains controversial. Optogenetic and chemogenetic tools offer the means to assess such integration. However, constructing modifiable iPSC-derived neurons requires efficient gene editing. Here, we used CRISPR/Cas9 (targeting the <i>AAVS1</i> safe harbor) and PiggyBac transposon systems to insert optogenetic and chemogenetic receptors (ChR2/hM4Di) into human iPSCs. While both systems successfully integrated genes into the genomes of HEK293T cells and iPSCs, receptor expression was detected only in HEK293T cells. Bisulfite sequencing revealed extensive methylation of the TRE3G BI promoter (95.3-98.2%) in iPSCs, in contrast to low methylation (5.9%) in HEK293T cells. For PiggyBac, the methylation of CMV/EF1α promoters in iPSCs exhibited integration site-dependent variability (0-95.2%). Notably, even hypomethylated clones failed to show gene expression, suggesting that additional regulatory mechanisms, such as histone modifications or chromatin remodeling, may contribute to transcriptional silencing. Differentiation into neural stem cells does not reverse methylation nor restore protein expression. Our findings demonstrate that the CRISPR/Cas9 and PiggyBac systems enable the integration of optochemical receptor genes into iPSCs. However, promoter methylation or other epigenetic and non-epigenetic gene-silencing mechanisms could pose barriers to efficient protein expression from the integrated transgene in iPSCs.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2606983"},"PeriodicalIF":3.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12758201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA MIR4435-2HG-mediated succinylation of USF1 promotes its protein stability and induces epithelial-mesenchymal transition in HNSCC.","authors":"Shujin He, Jing Wang, Dingding Wang, Wei Wang, Anjia Han, Honggang Liu","doi":"10.1080/15592294.2026.2672218","DOIUrl":"10.1080/15592294.2026.2672218","url":null,"abstract":"<p><p>Tumor recurrence and metastasis remain the principal causes of mortality in patients with head and neck squamous cell carcinoma (HNSCC). However, the key molecular drivers underlying HNSCC progression and their regulatory mechanisms have not yet been fully elucidated. In this study, we investigated the biological role of the long noncoding RNA MIR4435-2HG in HNSCC. Integrated analyses across multiple public databases demonstrated that MIR4435-2HG is significantly upregulated in HNSCC and is closely associated with pathological T stage, clinical stage, and histological grade. Through further bioinformatic screening and functional validation, upstream transcription factor 1 (USF1) was identified as a critical downstream effector of MIR4435-2HG. Mechanistically, MIR4435-2HG directly interacts with USF1 and promotes its protein stability by facilitating USF1 succinylation, thereby enhancing tumor cell migration and invasion through the induction of epithelial - mesenchymal transition. Moreover, dual-luciferase reporter assays and RT-qPCR analyses revealed that CREB1 transcriptionally upregulates MIR4435-2HG expression, establishing a positive feedback regulatory circuit. Collectively, our findings demonstrate that MIR4435-2HG promotes USF1 succinylation and stabilization, leading to the formation of a MIR4435-2HG - USF1-AKT - CREB1 signalling loop that drives epithelial - mesenchymal transition and facilitates the invasive and metastatic potential of HNSCC cells.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2672218"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13178182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147927716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CTCF delimits a DNA methylation transition at the intergenic region between the embryonic and adult α-globin genes.","authors":"Gustavo Tapia-Urzúa, Hober Nelson Núñez-Martínez, Sylvia Garza-Manero, Martin Franke, Carlos Alberto Peralta-Alvarez, Ángel Josué Cerecedo-Castillo, Georgina Guerrero, José Luis Gómez-Skarmeta, Félix Recillas-Targa","doi":"10.1080/15592294.2026.2711190","DOIUrl":"10.1080/15592294.2026.2711190","url":null,"abstract":"<p><p>Transcriptional activation of cell-type-specific genes is achieved by multiple mechanisms that guarantee chromatin accessibility at <i>cis</i>-regulatory elements and the long-range interactions between them. Generally, DNA methylation counteracts these processes and promotes gene silencing in vertebrates. CTCF is a conserved and essential multifunctional transcription factor relevant for establishing and maintaining chromatin architecture and accessibility, while its precise role in regulating DNA methylation remains to be determined. We focused on the highly abundant and previously studied erythroid-specific α^D gene (<i>HBAD</i>) to systematically investigate the role of CTCF binding on DNA methylation, chromatin accessibility, and gene expression using a chicken erythroid cell differentiation system. The perturbation of CTCF binding at the intergenic region between the embryonic π and the adult α^D gene resulted in DNA methylation propagation towards the α^D gene, which was accompanied by decreased chromatin accessibility, GATA-1 binding, and gene expression. Notably, chromatin conformation analyses revealed that CTCF binding enables α^D transcriptional activation independently of its architectural function. We observed a similar role of CTCF on DNA methylation and gene expression in the human orthologous gene <i>HBA2</i>. Our findings support a conserved role of CTCF in preventing DNA methylation spreading and gene silencing of cell-type-specific genes along differentiation.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2711190"},"PeriodicalIF":3.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13436835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}