Ask about this productRelated genes to: DNMT1 antibody
- Gene:
- DNMT1 NIH gene
- Name:
- DNA methyltransferase 1
- Previous symbol:
- DNMT
- Synonyms:
- MCMT, CXXC9
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-04
- Date modifiied:
- 2019-04-23
Related products to: DNMT1 antibody
Related articles to: DNMT1 antibody
- Diabetes mellitus (DM) and its complications represent a major global health burden, driven by a combination of genetic and environmental factors. Growing evidence indicates that epigenetic modifications, particularly DNA methylation, play a critical role in the pathogenesis of DM and its progression to complications such as diabetic cardiomyopathy, nephropathy, retinopathy, and impaired wound healing. DNA methyltransferases (DNMTs), including DNMT1, DNMT3A, and DNMT3B, are key enzymes responsible for establishing and maintaining DNA methylation patterns. Under diabetic conditions, hyperglycemia and metabolic dysregulation lead to aberrant expression and activity of DNMTs, resulting in methylation dysregulation of genes involved in insulin signalling, pancreatic islet β-cell function, oxidative stress, inflammation, and fibrosis. Although numerous studies have identified abnormal DNMT expression in diabetes and its complications, the precise mechanisms triggering DNMT dysregulation and its tissue-specific effects remain incompletely elucidated. This review summarises current advances in understanding the role of DNMTs in the pathogenesis of DM and its complications, discusses their therapeutic potential, and suggests that targeting DNMT-mediated epigenetic pathways may offer novel strategies for preventing and reversing diabetes and its associated complications. - Source: PubMed
Publication date: 2026/05/22
Zhang ShengnanDai ShupengLu ChenxiaLi LiWu YuxingchunChen Mi - Curcumin, a natural compound extracted from turmeric, has shown potential in modulating epigenetic mechanisms, including DNA methylation, which is critical in gene regulation and cancer progression. This study investigates the impact of curcumin on the methylation of DNMT1, CDH1, SMG1, and WT1 genes in the MIAPaCa2 pancreatic cancer cell line. - Source: PubMed
Publication date: 2026/05/01
Mousavi ShaghayeghAzad MehdiKarami Chermahini NedaPakbin BabakMomeni Abdolmabood - Radiation-induced heart disease (RIHD) is a serious adverse reaction after tumor radiotherapy; its molecular mechanism is not yet clear, and there is a lack of effective treatment strategies. DNA methyltransferase 1 (DNMT1) plays crucial roles in various biological processes, but its function in RIHD remains to be explored. This study aimed to systematically elucidate the molecular map of RIHD using multiomic methods, with a focus on the specific functions and mechanisms of DNMT1 in the development of RIHD. In this study, in vivo and in vitro models of radiation-induced cardiac injury were constructed. Changes in molecular expression in cardiac tissues and cells caused by radiation were systematically analyzed through techniques such as transcriptomics and proteomics. Adeno-associated virus and lentivirus transfection techniques were used to knock down Dnmt1 expression to explore its functional role in RIHD. Multiomic analysis revealed significant activation of immune/inflammatory responses and metabolic disorders in RIHD. X-ray irradiation induced myocardial tissue and cell damage and inhibited PI3K/PDK1/AKT signaling. Moreover, radiation significantly upregulated the expression of DNMT1 in myocardial tissue and cells. Dnmt1 knockdown alleviated radiation-induced myocardial tissue and cell damage and partially reversed the inhibition of PI3K/AKT signaling. In addition, 15 proteins directly interacting with DNMT1 were identified by CO-IP and GST-pulldown assays combined with mass spectrometry, suggesting that these proteins may participate in the development of RIHD through a variety of molecular mechanisms. The results of this study revealed that DNMT1 plays a role in promoting disease progression by regulating the PI3K/AKT signaling pathway in RIHD. These findings provide a new perspective for understanding the pathogenesis of RIHD and suggest that DNMT1 may serve as a potential target for therapeutic interventions. Therefore, DNMT1 represents a promising therapeutic target for preventing RIHD. - Source: PubMed
Wang GangLi Yan-LingWang Bo-WenWang RongWang YanShu Yan-BiaoZhang Wen-BoWu PanHu Yu-JieLu Wei-JieXie Ping - Renal fibrosis is a pathological feature of advanced-stage diabetic kidney disease (DKD). Here, we investigated the effect of Pirfenidone (PFD) on renal fibrosis under diabetic conditions and its molecular mechanism. Sirius red staining and immunohistochemistry were used for histological analysis in rat kidney. Levels of serum creatinine (Scr) and blood urea nitrogen (BUN) were detected by kits. Lipid hydroperoxide, malondialdehyde (MDA), glutathione peroxidase (GPX), and superoxide dismutase (SOD) were measured by commercial kits. Immunofluorescence staining was used to evaluate the expression and colocalization of USP7 and DNMT1. Mitochondrial and cytoplasmic reactive oxygen species (ROS) levels were detected. GLIS1, DNMT1, and USP7 mRNA were measured by RT-qPCR. Protein levels of DNMT1, USP7, fibronectin, p-Smad2, Smad2, p-Smad3, and Smad3 were detected by Western blot. Methylation of the GLIS1 promoter was assessed utilizing methylation-specific polymerase chain reaction (MSP). Chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (Co-IP) verified molecular interactions. PFD alleviated renal injury and fibrosis in DKD rats by suppressing TGF-β1/Smad signaling. PFD attenuated renal oxidative stress and mitochondrial dysfunction in DKD rats. GLIS1 knockdown reversed PFD's protective effects in high glucose (HG)-exposed HK-2 cells, abolishing its improvements in oxidative stress, mitochondrial function, and fibrosis. PFD attenuated HG-induced GLIS1 promoter hypermethylation by suppressing DNMT1 binding and activity, thereby restoring GLIS1 expression. PFD suppressed DNMT1 activity by disrupting USP7/DNMT1 complex. Importantly, the USP7/DNMT1 axis mediated the regulatory effect on GLIS1, which subsequently counteracted PFD's protective effects on HG-stimulated HK-2 cells. PFD upregulates GLIS1 by disrupting the USP7/DNMT1 complex, which subsequently suppresses the ROS/TGF-β1/Smad pathway to alleviate renal fibrosis in DKD. This study identifies the USP7/DNMT1/GLIS1 epigenetic axis as a critical upstream mechanism driving the protective effects of PFD, providing new therapeutic targets for DKD treatment. - Source: PubMed
Tu WeiHu LeiWu LitingZhou HongtaoYang RongChen Yanxia - The abnormal tumor vasculature can present a barrier to the infiltration of anti-tumor immune cells, which impairs immune surveillance and response to immunotherapy. Here, we show that genetically deleting the epigenetic factor DNA methyltransferase 1 (Dnmt1) in endothelial cells (ECs) reduces angiogenesis while imparting profound changes to the tumor immune microenvironment (TIME), including increased proportions of CD4 memory T cells and NK cells. Depleting CD4 T cells, or blocking lymphocyte egress from the lymph nodes, rescues tumor growth in mice with conditional deletion of Dnmt1 in ECs (Dnmt1) and dramatically shortens overall survival, whereas NK cells are dispensable. Tumors implanted in Dnmt1 mice show reduced vascular branching, elevated expression of VCAM1, increased vessel-associated T cells, and a shift in vascular specification, including increased proportions of immune-permissive post-capillary venules (PCVs) and interferon-stimulated ECs (IFN-ECs). Deleting Dnmt1 in EC cultures strikingly potentiates responses to combinations of IFNγ and TNFα and, notably, up-regulates important T-cell co-stimulatory molecules for memory CD4 T cells, including Icosl, Cd40, and Tnfsf4. Finally, immune checkpoint blockade (ICB) administered to Dnmt1 mice with experimental melanoma lung metastasis reduces tumor burden, with some mice showing tumor eradication. Our findings identify endothelial Dnmt1 as a key regulator of vascular-mediated anti-tumor immunity, providing a rationale for integrating epigenetic modulation of the vasculature with cancer immunotherapy regimens. - Source: PubMed
Publication date: 2026/05/19
Kim Dae JoongMcGinty MitchellAnandh SwethaRiedstra CarolineSethi YuvrajRutkowski Melanie RDudley Andrew C