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Journal articles on the topic 'DNA methylation'

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Published: 4 June 2021
Last updated: 7 July 2024

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1

Mikaelsson, Mikael A., and Courtney A. Miller. "DNA methylation." Epigenetics 6, no. 5 (May 2011): 548–51. http://dx.doi.org/10.4161/epi.6.5.15679.

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2

Singal, Rakesh, and Gordon D. Ginder. "DNA Methylation." Blood 93, no. 12 (June 15, 1999): 4059–70. http://dx.doi.org/10.1182/blood.v93.12.4059.

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3

Singal, Rakesh, and Gordon D. Ginder. "DNA Methylation." Blood 93, no. 12 (June 15, 1999): 4059–70. http://dx.doi.org/10.1182/blood.v93.12.4059.412k40_4059_4070.

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4

Dang, Pengtao, Xiao Wang, Haiqi Zhu, Jia Wang, Tingbo Guo, Xinyu Zhou, Paveethran Swaminathan, Chi Zhang, and Sha Cao. "Abstract 5352: Targeting DNA methylation in T cells to improve the efficacy of immunotherapy." Cancer Research 83, no. 7_Supplement (April 4, 2023): 5352. http://dx.doi.org/10.1158/1538-7445.am2023-5352.

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Abstract T-cells are critical mediators of immunity and immunologic memory. Their cell fates are regulated in part through epigenetic mechanisms, including DNA methylation. Recent genome-wide methylation analyses have revealed dynamic alterations in the methylome at various stages of development and differentiation of T cells. At single cell level, it is not easy to simultaneously collect RNA-seq and RBBS methylation profiling. An important task is to understand the expression change of which genes and pathways are regulated by DNA methylations, especially for the ones that are associated with functional variations in the T cells from tumor microenvironment.In this study, we developed a computational approach based on our recently developed metabolic flux estimation to estimate cell-wise global DNA methylation activity level by using scRNA-seq data. We also hypothesize that the global DNA methylation activity level in one cell determines most of the DNA methylation level in gene-specific DNA methylations. Hence, the dependency between gene-specific DNA methylation and expression could be imputed by the dependency between predicted global DNA methylation input level and the gene expression. We validated our method to impute cell-wise global DNA methylation level by using four independent sets of paired gene expression and DNA methylation data. Noted, our prediction of global DNA methylation activity is from a pure metabolic perspective. We found that two metabolic reaction rates, named metabolic flux from methionine to SAM and SAM to SAH, purely predicted by using gene expression data can accurately impute DNA methylation activity in all validating data sets. Our method enables further identification of the disease/cell context specific contributor of DNA methylation, i.e., the genes high contribution to DNA methylations in each individual cell or cell groups. We applied our method on scRNA-seq data of different T cell types extracted from TME of lung, liver, and colon cancer. We have seen that exhausted T cells, especially the ones with decreased Granzymes and PRF1 are associated with increased global DNA methylation level and related genes, suggesting the potential clinical implications in targeting DNA methylation to improve the efficacy of immunotherapies. Citation Format: Pengtao Dang, Xiao Wang, Haiqi Zhu, Jia Wang, Tingbo Guo, Xinyu Zhou, Paveethran Swaminathan, Chi Zhang, Sha Cao. Targeting DNA methylation in T cells to improve the efficacy of immunotherapy. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5352.
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5

KARAASLAN, Ezgi, Ceren ACAR, and Şükrü KARTALCI. "Şizofrenide Epigenetik Bakış Açısı: DNA Metilasyon Modelleri." Arşiv Kaynak Tarama Dergisi 31, no. 3 (September 30, 2022): 204–12. http://dx.doi.org/10.17827/aktd.1096901.

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Schizophrenia is a mental disorder characterized by delusions, hallucinations and various behavioral disorders. Affecting approximately 1% of the world's population, schizophrenia not only affects patients, but also other members of the society. Genetic and environmental factors play roles in the etiology of the disorder.Genetics, neurodevelopmental disorder, drug use, urban life, alone or together can be counted as the factors that cause the disorder. Despite increasing studies in recent years, the factors causing the formation of schizophrenia have not been fully clarified and more research is needed. Although genetic factors are risk factors for schizophrenia, it is thought that some environmental factors affect the emergence of the disorder. Epigenetic mechanisms regulate gene functions without changing the nucleotide sequence of DNA. DNA methylation is associated with schizophrenia, and methylation status studies have been conducted in many schizophrenia candidate genes. Examination of DNA methylation states will contribute significantly to psychiatric research.In this review, data published in global databases obtained from DNA methylation studies related with schizophrenia are summarized and their importance in schizophrenia is briefly discussed.
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6

Sermswan, R., S. Mongkolsuk, and S. Sirisinha. "Characterization of the Opisthorchis viverrini genome." Journal of Helminthology 65, no. 1 (March 1991): 51–54. http://dx.doi.org/10.1017/s0022149x00010439.

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ABSTRACTThe methylations of trematode genomic DNA were analyzed using restriction enzymes and Southern blot hybridization. Restriction enzymes MspI, HpaII, HhaI were used to probe CpG methylation while MboI, Sau3A, DpnI were used for A methylation. The results revealed that Opisthorchis viverrini, Fasciola gigantica and Gigantocotyle siamensis had neither CpG nor A methylations. The presence of highly repeated DNA elements was also demonstrated in O. viverrini genomic DNA.
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7

Okitsu, Cindy Yen, and Chih-Lin Hsieh. "DNA Methylation Dictates Histone H3K4 Methylation." Molecular and Cellular Biology 27, no. 7 (January 22, 2007): 2746–57. http://dx.doi.org/10.1128/mcb.02291-06.

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ABSTRACT Histone lysine methylation and DNA methylation contribute to transcriptional regulation. We have previously shown that acetylated histones are associated with unmethylated DNA and are nearly absent from the methylated DNA regions by using patch-methylated stable episomes in human cells. The present study further demonstrates that DNA methylation immediately downstream from the transcription start site has a dramatic impact on transcription and that DNA methylation has a larger effect on transcription elongation than on initiation. We also show that dimethylated histone H3 at lysine 4 (H3K4me2) is depleted from regions with DNA methylation and that this effect is not linked to the transcriptional activity in the region. This effect is a local one and does not extend even 200 bp from the methylated DNA regions. Although depleted primarily from the methylated DNA regions, the presence of trimethylated histone H3 at lysine 4 (H3K4me3) may be affected by transcriptional activity as well. The data here suggest that DNA methylation at the junction of transcription initiation and elongation is most critical in transcription suppression and that this effect is mechanistically mediated through chromatin structure. The data also strongly support the model in which DNA methylation and not transcriptional activity dictates a closed chromatin structure, which excludes H3K4me2 and H3K4me3 in the region, as one of the pathways that safeguards the silent state of genes.
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8

Vogelgsang, Lars, Azlan Nisar, Sebastian Alexander Scharf, Anna Rommerskirchen, Dana Belick, Alexander Dilthey, and Birgit Henrich. "Characterisation of Type II DNA Methyltransferases of Metamycoplasma hominis." Microorganisms 11, no. 6 (June 15, 2023): 1591. http://dx.doi.org/10.3390/microorganisms11061591.

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Bacterial virulence, persistence and defence are affected by epigenetic modifications, including DNA methylation. Solitary DNA methyltransferases modulate a variety of cellular processes and influence bacterial virulence; as part of a restriction-modification (RM) system, they act as a primitive immune system in methylating the own DNA, while unmethylated foreign DNA is restricted. We identified a large family of type II DNA methyltransferases in Metamycoplasma hominis, comprising six solitary methyltransferases and four RM systems. Motif-specific 5mC and 6mA methylations were identified with a tailored Tombo analysis on Nanopore reads. Selected motifs with methylation scores >0.5 fit with the gene presence of DAM1 and DAM2, DCM2, DCM3, and DCM6, but not for DCM1, whose activity was strain-dependent. The activity of DCM1 for CmCWGG and of both DAM1 and DAM2 for GmATC was proven in methylation-sensitive restriction and finally for recombinant rDCM1 and rDAM2 against a dam-, dcm-negative background. A hitherto unknown dcm8/dam3 gene fusion containing a (TA) repeat region of varying length was characterized within a single strain, suggesting the expression of DCM8/DAM3 phase variants. The combination of genetic, bioinformatics, and enzymatic approaches enabled the detection of a huge family of type II DNA MTases in M. hominis, whose involvement in virulence and defence can now be characterized in future work.
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9

Whalley, Katherine. "Dynamic DNA methylation." Nature Reviews Neuroscience 8, no. 5 (April 4, 2007): 323. http://dx.doi.org/10.1038/nrn2133.

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10

Meissner, Alexander. "Guiding DNA Methylation." Cell Stem Cell 9, no. 5 (November 2011): 388–90. http://dx.doi.org/10.1016/j.stem.2011.10.014.

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11

Stower, Hannah. "Dynamic DNA methylation." Nature Reviews Genetics 13, no. 2 (January 4, 2012): 75. http://dx.doi.org/10.1038/nrg3156.

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12

Muers, Mary. "Disentangling DNA methylation." Nature Reviews Genetics 14, no. 8 (June 25, 2013): 519. http://dx.doi.org/10.1038/nrg3535.

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13

Issa, Jean-Pierre J., and Hagop M. Kantarjian. "Targeting DNA Methylation." Clinical Cancer Research 15, no. 12 (June 9, 2009): 3938–46. http://dx.doi.org/10.1158/1078-0432.ccr-08-2783.

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14

Wang, Heng, Yumo Xie, Gaopo Xu, Xiaolin Wang, Meijin Huang, Yanxin Luo, and Huichuan Yu. "Abstract 5272: Aberrant DNA 5mC and 6mA methylations increase ACE2 expression in intestinal cancer cells susceptible to SARS-CoV-2 infection." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5272. http://dx.doi.org/10.1158/1538-7445.am2022-5272.

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Abstract Angiotensin converting enzyme II (ACE2) is the cellular receptor of SARS-CoV-2. At present, ACE2 receptor is considered to be the key component in the SARS-CoV-2 infection and transmitting in the host. Among the cancer patients with COVID-19, the gastrointestinal cancer is the second most prevalent. The MethyLight and QASM assays were used to evaluated the genomic DNA 5mC methylation, while the CviAII enzyme-based 6mA-RE-qPCR was applied to determine motif-specific DNA 6mA methylation. The 6mA and 5mC methylation analyses of the long interspersed nuclear elements 1 (LINE1) were used to evaluate the global level of genomic 6mA and 5mC methylations, respectively. To investigate the role of ACE2 DNA methylation in regulating ACE2 expression, we performed a genome-wide methylation analysis in colorectal cancer samples collected at the Sixth Affiliated Hospital of Sun Yat-sen University. The DNA 5mC methylation of ACE2 promoter in tumor tissues were significantly lower than that in normal tissues, while the DNA 6mA methylation of ACE2 promoter in tumor tissues was significantly higher than that in normal tissues. In addition, the mRNA and protein expression of ACE2 in tumor tissues were lower than that in normal tissues. To explore the epigenetic regulation on ACE2 expression, we treated colon cancer cell lines with 5-Azacytidine and found ACE2 expression was upregulated after lowering the DNA 5mC methylation. The correlation analysis in patient cohort samples showed that ACE2 mRNA expression was positively correlated with DNA 5mC and negatively associated with DNA 6mA methylation. Next, a novel CRISPR-based tool was developed for sequence-specific 6mA editing on ACE2 promoter region, and it was applied in HCT116 cell to further confirm the regulatory role of DNA 6mA methylation in ACE2 mRNA expression. This tool was proved to be reliable with our findings that the CRISPR/dCas9-METTL3 tool could dramatically upregulate DNA 6mA methylation in ACE2 promoter, while the global level of genomic 6mA methylation remained unchanged. Both the mRNA and protein expression of ACE2 were significantly increased following a sequence-specific DNA 6mA editing in ACE2 promoter. In conclusion, we revealed the aberrant DNA 5mC and 6mA methylations in colorectal cancer, which upregulate ACE2 expression in colorectal cancer cells that may confer the susceptibility to SARS-CoV-2 infection. We developed a novel CRISPR-based tool that could realize site-directed 6mA methylation editing. Notably, the epigenetic regulation of DNA 6mA methylation on ACE2 expression provides an insight into the intersection of the biology of cancer, SARS-CoV-2 infection and organ-specific complication in COVID-19. Aberrant ACE2 methylation may serve as a biomarker and treatment target in these patients. Citation Format: Heng Wang, Yumo Xie, Gaopo Xu, Xiaolin Wang, Meijin Huang, Yanxin Luo, Huichuan Yu. Aberrant DNA 5mC and 6mA methylations increase ACE2 expression in intestinal cancer cells susceptible to SARS-CoV-2 infection [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5272.
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15

Majchrzak-Celińska, A., M. Naskret-Barciszewska, M. Giel-Pietraszuk, W. Nowak, P. Śron, and A. Barciszewska. "P02.08.A The relations of focal and total DNA methylation in gliomas." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii31. http://dx.doi.org/10.1093/neuonc/noac174.101.

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Abstract Background The role of epigenetic events in gliomagenesis is undoubtful. However, the role of specific pathological events is not so clear. It was shown that loss in total DNA methylation correlates with higher tumor malignancy and oxidative DNA damage. But promoter methylation of many genes was reported to be significant for gliomas’ malignancy and predictive for the treatment outcome. In carcinogenesis in general global DNA hypomethylation and focal hypermethylation coexist. The aim of our project was to evaluate the correlation between total DNA methylation and promoter methylation of selected genes. Material and Methods We analysed glioma tissues from 60 patients. For total DNA methylation analysis we used the radiolabelling method with TLC separation of nucleotides and content estimation with phosphoimager. For promoter methylation analysis we have chosen: MGMT (O-6-Methylguanine-DNA Methyltransferase), MPG (DNA-3-methyladenine glycosylase), GJA1 (Gap junction alpha-1 protein / connexin 43). The promoter methylation level was evaluated with the methylation-sensitive high-resolution melting (MS-HRM) method. Results Total DNA methylation was reversely correlated with brain tumor grade, confirming that 5-methylcytosine loss is important step in gliomagenesis. From 3 genes only MPG promoter methylation showed clear low reverse correlation with tumor grade. Promoter methylation in GJA1 show low correlation with both, MGMT and MPG, but there was no link between MGMT and MPG. IDHwt presence was significantly correlated with higher tumor grade. Promoter methylations in MPG and GJA1 were better correlated with IDH status than in MGMT. Conclusion There is a clear correlation between total DNA methylation and tumor malignancy. Gene promoter methylation is not highly correlated with total DNA methylation and shows low significance in selected cases. Promoter methylation showed clear correlation with tumor grade only in MPG case. That suggests diverse mechanisms steering DNA methylation in general and local changes. It also shows that total DNA methylation is best predictor of tumor grade.
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16

Huang, Yung-Hsin, Su Jianzhong, Yong Lei, Michael C. Gundry, Xiaotian Zhang, Mira Jeong, Wei Li, and Margaret A. Goodell. "DNA Epigenome Editing Using Crispr-Cas Suntag-Directed DNMT3A." Blood 128, no. 22 (December 2, 2016): 2707. http://dx.doi.org/10.1182/blood.v128.22.2707.2707.

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Abstract DNA methylation, an epigenetic modification, has widespread effects on gene expression during development. However, our ability to assign specific function to regions of DNA methylation is limited by the poor correlation between global patterns of DNA methylation and gene expression. To overcome this barrier, we utilized nuclease-deactivated Cas9 protein fused to repetitive peptide epitopes (SunTag) recruiting multiple copies of antibody-fused de novo DNA methyltranferase 3A (DNMT3A) (CRISPR-Cas SunTag-directed DNMT3A) to amplify local DNMT3A concentration and to methylate genomic sites of interest. Here, we demonstrated that CRISPR-Cas SunTag-directed DNMT3A not only dramatically increased CpG methylation but also, to our surprise, CpH (H =A or C or T) methylation at the HOXA5 lociin human embryonic kidney 293T cells (HEK293T). Furthermore, using a single sgRNA, CRISPR-Cas SunTag-directed DNMT3A was capable of methylating 4.5 kb genomic regions, surpassing previous targeted methylation tools whose activity is limited to 200bp. Using reduced representation bisulfite sequencing (RRBS) and RNA-seq, we concluded that CRISPR-Cas SunTag-directed DNMT3A methylated regions of interest without affecting global DNA methylome and transcriptome. This effective and precise tool enables site-specific manipulation of DNA methylation and may be used to address the relationship beteween DNA methylation and gene expression. Disclosures No relevant conflicts of interest to declare.
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17

Gonçalves, Ana Cristina, Raquel Alves, Inês Baldeiras, Bárbara Marques, Bárbara Oliveiros, Amélia Pereira, José Manuel Nascimento Costa, Emília Cortesão, Luisa Mota Vieira, and Ana Bela Sarmento Ribeiro. "DNA Methylation Is Correlated with Oxidative Stress in Myelodysplastic Syndrome—Relevance as Complementary Prognostic Biomarkers." Cancers 13, no. 13 (June 23, 2021): 3138. http://dx.doi.org/10.3390/cancers13133138.

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Oxidative stress and abnormal DNA methylation have been implicated in cancer, including myelodysplastic syndromes (MDSs). This fact leads us to investigate whether oxidative stress is correlated with localized and global DNA methylations in the peripheral blood of MDS patients. Sixty-six MDS patients and 26 healthy individuals were analyzed. Several oxidative stress and macromolecule damage parameters were analyzed. Localized (gene promotor) and global DNA methylations (5-mC and 5-hmC levels; LINE-1 methylation) were assessed. MDS patients had lower levels of reduced glutathione and total antioxidant status (TAS) and higher levels of peroxides, nitric oxide, peroxides/TAS, and 8-hydroxy-2-deoxyguanosine compared with controls. These patients had higher 5-mC levels and lower 5-hmC/5-mC ratio and LINE-1 methylation and increased methylation frequency of at least one methylated gene. Peroxide levels and peroxide/TAS ratio were higher in patients with methylated genes than those without methylation and negatively correlated with LINE-1 methylation and positively with 5-mC levels. The 5-hmC/5-mC ratio was significantly associated with progression to acute leukemia and peroxide/TAS ratio with overall survival. This study points to a relationship between oxidative stress and DNA methylation, two common pathogenic mechanisms involved in MDS, and suggests the relevance of 5-hmC/5-mC and peroxide/TAS ratios as complementary prognostic biomarkers.
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18

Wang, Mengchi, Kai Zhang, Vu Ngo, Chengyu Liu, Shicai Fan, John W. Whitaker, Yue Chen, et al. "Identification of DNA motifs that regulate DNA methylation." Nucleic Acids Research 47, no. 13 (June 25, 2019): 6753–68. http://dx.doi.org/10.1093/nar/gkz483.

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AbstractDNA methylation is an important epigenetic mark but how its locus-specificity is decided in relation to DNA sequence is not fully understood. Here, we have analyzed 34 diverse whole-genome bisulfite sequencing datasets in human and identified 313 motifs, including 92 and 221 associated with methylation (methylation motifs, MMs) and unmethylation (unmethylation motifs, UMs), respectively. The functionality of these motifs is supported by multiple lines of evidence. First, the methylation levels at the MM and UM motifs are respectively higher and lower than the genomic background. Second, these motifs are enriched at the binding sites of methylation modifying enzymes including DNMT3A and TET1, indicating their possible roles of recruiting these enzymes. Third, these motifs significantly overlap with “somatic QTLs” (quantitative trait loci) of methylation and expression. Fourth, disruption of these motifs by mutation is associated with significantly altered methylation level of the CpGs in the neighbor regions. Furthermore, these motifs together with somatic mutations are predictive of cancer subtypes and patient survival. We revealed some of these motifs were also associated with histone modifications, suggesting a possible interplay between the two types of epigenetic modifications. We also found some motifs form feed forward loops to contribute to DNA methylation dynamics.
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19

Wei, Zhen, Subbarayalu Panneerdoss, Santosh Timilsina, Jingting Zhu, Tabrez A. Mohammad, Zhi-Liang Lu, João Pedro de Magalhães, et al. "Topological Characterization of Human and Mouse m5C Epitranscriptome Revealed by Bisulfite Sequencing." International Journal of Genomics 2018 (June 13, 2018): 1–19. http://dx.doi.org/10.1155/2018/1351964.

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Background. Compared with the well-studied 5-methylcytosine (m5C) in DNA, the role and topology of epitranscriptome m5C remain insufficiently characterized. Results. Through analyzing transcriptome-wide m5C distribution in human and mouse, we show that the m5C modification is significantly enriched at 5′ untranslated regions (5′UTRs) of mRNA in human and mouse. With a comparative analysis of the mRNA and DNA methylome, we demonstrate that, like DNA methylation, transcriptome m5C methylation exhibits a strong clustering effect. Surprisingly, an inverse correlation between mRNA and DNA m5C methylation is observed at CpG sites. Further analysis reveals that RNA m5C methylation level is positively correlated with both RNA expression and RNA half-life. We also observed that the methylation level of mitochondrial RNAs is significantly higher than RNAs transcribed from the nuclear genome. Conclusions. This study provides an in-depth topological characterization of transcriptome-wide m5C modification by associating RNA m5C methylation patterns with transcriptional expression, DNA methylations, RNA stabilities, and mitochondrial genome.
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Altaf, Adil, and Ahmad Zada. "DNA METHYLATION IN PLANTS." Journal of Global Innovations in Agriculture Sciences 9, no. 3 (September 27, 2021): 109–14. http://dx.doi.org/10.22194/jgias/9.954.

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Common DNA methylation controls gene expression and preserves genomic integrity. Mal methylation can cause developmental abnormalities in the plants. Multiple enzymes carrying out de novo methylation, methylation maintenance, and active demethylation culminate in a particular DNA methylation state. Next-generation sequencing advances and computational methods to analyze the data. The model plant Arabidopsis thaliana was used to study DNA methylation patterns, epigenetic inheritance, and plant methylation. Plant DNA methylation research reveals methylation patterns and describing variations in plant tissues. Determining the kinetics of DNA methylation in diverse plant tissues is also a new field. However, it is vital to understand regulatory and developmental decisions and use plant model species to develop new commercial crops; that are more resistant to stress and yield more. There are several methods available for assessing DNA methylation data. The performance of several techniques is assessed in A. thaliana, which has a smaller genome than hexaploid bread wheat. Keywords: DNA methylation, plants, process, use and benefits.
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Nitin, Mukesh. "DNA METHYLATION SEQUENCING: A PROMISING TOOL FOR PANCREATIC CANCER DIAGNOSIS." Indian Journal of Health Care Medical & Pharmacy Practice 5, no. 1 (May 25, 2024): 103–11. http://dx.doi.org/10.59551/ijhmp/25832069/2024.5.1.140.

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Pancreatic cancer remains a deadly disease due to late diagnosis and limited treatment options. DNA methylation, a key epigenetic modification, plays a crucial role in cancer development and progression. Various research using DNA methylation patterns in pancreatic cancer tissues resulted in comparative evaluation of normal pancreas and cell lines resulted in the identification of potential biomarkers for diagnosis and therapy. During DNA methylation case studies led to identification 807 genes and 1505 CpG sites. Also, 289 differentially methylated CpG sites were also reported suggesting their vital contribution towards pancreatic cancer. In current review tried to explore the methylation approaches to identify important genes linked to gemcitabine, a common chemotherapy drug, identifying potential markers for patient response. This study sheds light on the link between DNA methylation and pancreatic cancer, paving the way for novel therapeutic targets and improved patient outcomes.
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Li, W., A. Van Soom, and L. Peelman. "Repeats as global DNA methylation marker in bovine preimplantation embryos." Czech Journal of Animal Science 62, No. 2 (February 6, 2017): 43–50. http://dx.doi.org/10.17221/29/2016-cjas.

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DNA methylation undergoes dynamic changes and is a crucial part of the epigenetic regulation during mammalian early development. To determine the DNA methylation levels in bovine embryos, we applied a bisulfite sequencing based method aimed at repetitive sequences including three retrotransposons (L1_BT, BovB, and ERV1-1-I_BT) and Satellite I. A more accurate estimate of the global DNA methylation level compared to previous methods using only one repeat sequence, like Alu, could be made by calculation of the weighted arithmetic mean of multiple repetitive sequences, considering the copy number of each repetitive sequence. Satellite I and L1_BT showed significant methylation reduction at the blastocyst stage, while BovB and ERV1-1-I_BT showed no difference. The mean methylation level of the repetitive sequences during preimplantation development was the lowest at the blastocyst stage. No methylation difference was found between embryos cultured in 5% and 20% O<sub>2</sub>. Because mutations of CpGs negatively influence the calculation accuracy, we checked the mutation rate of the sequenced CpG sites. Satellite I and L1_BT showed a relatively low mutation rate (1.92 and 3.72% respectively) while that of ERV1-1-I_BT and BovB was higher (11.95 and 24% respectively). Therefore we suggest using a combination of repeats with low mutation rate, taking into account the proportion of each sequence, as a relatively quick marker for the global DNA methylation status of preimplantation stages and possibly also for other cell types.
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Osakabe, Akihisa, Fumiya Adachi, Yasuhiro Arimura, Kazumitsu Maehara, Yasuyuki Ohkawa, and Hitoshi Kurumizaka. "Influence of DNA methylation on positioning and DNA flexibility of nucleosomes with pericentric satellite DNA." Open Biology 5, no. 10 (October 2015): 150128. http://dx.doi.org/10.1098/rsob.150128.

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DNA methylation occurs on CpG sites and is important to form pericentric heterochromatin domains. The satellite 2 sequence, containing seven CpG sites, is located in the pericentric region of human chromosome 1 and is highly methylated in normal cells. In contrast, the satellite 2 region is reportedly hypomethylated in cancer cells, suggesting that the methylation status may affect the chromatin structure around the pericentric regions in tumours. In this study, we mapped the nucleosome positioning on the satellite 2 sequence in vitro and found that DNA methylation modestly affects the distribution of the nucleosome positioning. The micrococcal nuclease assay revealed that the DNA end flexibility of the nucleosomes changes, depending on the DNA methylation status. However, the structures and thermal stabilities of the nucleosomes are unaffected by DNA methylation. These findings provide new information to understand how DNA methylation functions in regulating pericentric heterochromatin formation and maintenance in normal and malignant cells.
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CAPLAKOVA, VERONIKA, EVA BABUSIKOVA, EVA BLAHOVCOVA, TOMAS BALHAREK, MARIA ZELIESKOVA, and JOZEF HATOK. "DNA Methylation Machinery in the Endometrium and Endometrial Cancer." Anticancer Research 36, no. 9 (September 9, 2016): 4407–20. http://dx.doi.org/10.21873/anticanres.10984.

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25

Cusack, Martin, and Paul Scotting. "DNA methylation in germ cell tumour aetiology: current understanding and outstanding questions." REPRODUCTION 146, no. 2 (August 2013): R49—R60. http://dx.doi.org/10.1530/rep-12-0382.

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Germ cell tumours (GCTs) are a diverse group of neoplasms that can be histologically subclassified as either seminomatous or non-seminomatous. These two subtypes have distinct levels of differentiation and clinical characteristics, the non-seminomatous tumours being associated with poorer prognosis. In this article, we review how different patterns of aberrant DNA methylation relate to these subtypes. Aberrant DNA methylation is a hallmark of all human cancers, but particular subsets of cancers show unusually high frequencies of promoter region hypermethylation. Such a ‘methylator phenotype’ has been described in non-seminomatous tumours. We discuss the possible cause of distinct methylation profiles in GCTs and the potential of DNA methylation to provide new targets for therapy. We also consider how recent developments in our understanding of this epigenetic modification and the development of genome-wide technologies are shedding new light on the role of DNA methylation in cancer aetiology.
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Das, Partha M., and Rakesh Singal. "DNA Methylation and Cancer." Journal of Clinical Oncology 22, no. 22 (November 15, 2004): 4632–42. http://dx.doi.org/10.1200/jco.2004.07.151.

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DNA methylation is an important regulator of gene transcription, and its role in carcinogenesis has been a topic of considerable interest in the last few years. Alterations in DNA methylation are common in a variety of tumors as well as in development. Of all epigenetic modifications, hypermethylation, which represses transcription of the promoter regions of tumor suppressor genes leading to gene silencing, has been most extensively studied. However, global hypomethylation has also been recognized as a cause of oncogenesis. New information concerning the mechanism of methylation and its control has led to the discovery of many regulatory proteins and enzymes. The contribution of dietary folate and methylene terahydrofolate reductase polymorphisms to methylation patterns in normal and cancer tissues is under intense investigation. As methylation occurs early and can be detected in body fluids, it may be of potential use in early detection of tumors and for determining the prognosis. Because DNA methylation is reversible, drugs like 5′-azacytidine, decitabine, and histone deacetylase inhibitors are being used to treat a variety of tumors. Novel demethylating agents such as antisense DNA methyl transferase and small interference RNA are being developed, making the field of DNA methylation wider and more exciting.
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Panjarian, Shoghag, and Jean-Pierre J. Issa. "The Roles of DNA Demethylases in Triple-Negative Breast Cancer." Pharmaceuticals 14, no. 7 (June 29, 2021): 628. http://dx.doi.org/10.3390/ph14070628.

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Triple-negative breast cancers (TNBCs) are very heterogenous, molecularly diverse, and are characterized by a high propensity to relapse or metastasize. Clinically, TNBC remains a diagnosis of exclusion by the lack of hormone receptors (Estrogen Receptor (ER) and Progesterone Receptor (PR)) as well as the absence of overexpression and/or amplification of HER2. DNA methylation plays an important role in breast cancer carcinogenesis and TNBCs have a distinct DNA methylation profile characterized by marked hypomethylation and lower gains of methylations compared to all other subtypes. DNA methylation is regulated by the balance of DNA methylases (DNMTs) and DNA demethylases (TETs). Here, we review the roles of TETs as context-dependent tumor-suppressor genes and/or oncogenes in solid tumors, and we discuss the current understandings of the oncogenic role of TET1 and its therapeutic implications in TNBCs.
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Saadatmand, Forough, Muneer Abbas, Victor Apprey, Krishma Tailor, and Bernard Kwabi-Addo. "Sex differences in saliva-based DNA methylation changes and environmental stressor in young African American adults." PLOS ONE 17, no. 9 (September 6, 2022): e0273717. http://dx.doi.org/10.1371/journal.pone.0273717.

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Background Low socioeconomic status neighborhood exposure to stress and violence may be sources of negative stimuli that poses significant health risks for children, adolescents and throughout the life course of an individual. The study aims to investigate if aberrant epigenetic DNA methylation changes may be a potential mechanism for regulating neighborhood exposures and health outcomes. Methods Exposure to environmental stressors identified in 98 young African American (AA) adults aged 18–25 years old from the Washington D.C., area were used in the study. We correlated the association between stress markers; cortisol, CRP, IgG, IGA, IgM, and self-reported exposure to violence and stress, with quantitative DNA methylation changes in a panel of gene-specific loci using saliva DNA. Results In all participants studied, the exposure to violence was significant and negatively correlated with DNA methylation of MST1R loci (p = 0.032; r = -0.971) and nominally significant with NR3C1 loci (p = 0.053; r = -0.948). In addition, we observed significant and negative correlation of DNA methylation changes of LINE1 (p = 0.044; r = -0.248); NR3C1 (p = 0.017; r = -0.186); MSTR1 (p = 0.022; r = -0.192); and DRD2 (p = 0.056; r = -0.184; albeit nominal significant correlation) with IgA expression. On the other hand, we observed a significant and position correlation of DNA methylation changes in DRD2 (p = 0.037; r = 0.184) with IgG expression. When participants were stratified by sex, we observed in AA young male adults, significant DNA methylation changes of MST1R (p< 0.05) and association with exposure to violence and IgG level. We also observed significant DNA methylation levels of DRD2 (p< 0.05) and association with IgA, IgG, and cortisol level. Furthermore, we observed significant DNA methylation changes of NR3C1 (p< 0.05) with stress, IgA, and IgG in the male participants only. On the other hand, we only observed significant and a positive association of IgG with DNA methylation levels of ESR1 (p = 0.041) in the young AA female participants. Conclusion Our preliminary observation of significant DNA methylation changes in neuronal and immune genes in saliva samples supports our recently published genome-wide DNA methylations changes in blood samples from young AA male adults indicating that saliva offers a non-invasive means for DNA methylation prediction of exposure to environmental stressors in a gender-specific manner.
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29

Meng, Huan X., James A. Hackett, Colm Nestor, Donncha S. Dunican, Monika Madej, James P. Reddington, Sari Pennings, David J. Harrison, and Richard R. Meehan. "Apoptosis and DNA Methylation." Cancers 3, no. 2 (April 1, 2011): 1798–820. http://dx.doi.org/10.3390/cancers3021798.

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30

Kim, Jei, Jee-Yeon Kim, and Jean-Pierre J. Issa. "Aging and DNA Methylation." Current Chemical Biology 3, no. 1 (January 1, 2009): 321–29. http://dx.doi.org/10.2174/187231309787158226.

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31

Kim, Jei, Jee-Yeon Kim, and Jean-Pierre Issa. "Aging and DNA Methylation." Current Chemical Biology 3, no. 1 (January 1, 2009): 1–9. http://dx.doi.org/10.2174/2212796810903010001.

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32

Shu, Yachun. "Insight into DNA Methylation." Journal of Drug Delivery and Therapeutics 9, no. 2 (March 15, 2019): 397–99. http://dx.doi.org/10.22270/jddt.v9i2.2419.

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33

Pokrywka, Małgorzata, Beata Kieć-Wilk, Anna Polus, and Iwona Wybrańska. "DNA methylation in obesity." Postępy Higieny i Medycyny Doświadczalnej 68 (November 27, 2014): 1383–91. http://dx.doi.org/10.5604/17322693.1130084.

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34

Hollander, Wouter, and Ingrid Meulenbelt. "DNA Methylation in Osteoarthritis." Current Genomics 16, no. 6 (September 7, 2015): 419–26. http://dx.doi.org/10.2174/1389202916666150817212711.

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35

PINARBAŞI, Ergün. "DNA Methylation in Eukaryotes." Turkish Journal of Biology 21, no. 4 (January 1, 1997): 515–23. http://dx.doi.org/10.55730/1300-0152.2497.

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36

Mahfouz, Magdy M. "RNA-directed DNA methylation." Plant Signaling & Behavior 5, no. 7 (July 2010): 806–16. http://dx.doi.org/10.4161/psb.5.7.11695.

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37

Michalowsky, L. A., and P. A. Jones. "DNA methylation and differentiation." Environmental Health Perspectives 80 (March 1989): 189–97. http://dx.doi.org/10.1289/ehp.8980189.

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38

Hitchins, Megan P., and Robyn L. Ward. "Favoritism in DNA Methylation." Cancer Prevention Research 2, no. 10 (September 29, 2009): 847–49. http://dx.doi.org/10.1158/1940-6207.capr-09-0178.

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39

Erdmann, Robert M., and Colette L. Picard. "RNA-directed DNA Methylation." PLOS Genetics 16, no. 10 (October 8, 2020): e1009034. http://dx.doi.org/10.1371/journal.pgen.1009034.

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40

Dong, Chunming, Woohyun Yoon, and Pascal J. Goldschmidt-Clermont. "DNA Methylation and Atherosclerosis." Journal of Nutrition 132, no. 8 (August 1, 2002): 2406S—2409S. http://dx.doi.org/10.1093/jn/132.8.2406s.

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Li, E., and Y. Zhang. "DNA Methylation in Mammals." Cold Spring Harbor Perspectives in Biology 6, no. 5 (May 1, 2014): a019133. http://dx.doi.org/10.1101/cshperspect.a019133.

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42

Mao, Steve. "DNA methylation promotes transcription." Science 362, no. 6419 (December 6, 2018): 1124.4–1124. http://dx.doi.org/10.1126/science.362.6419.1124-d.

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43

Finnegan, E. J., R. K. Genger, W. J. Peacock, and E. S. Dennis. "DNA METHYLATION IN PLANTS." Annual Review of Plant Physiology and Plant Molecular Biology 49, no. 1 (June 1998): 223–47. http://dx.doi.org/10.1146/annurev.arplant.49.1.223.

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Bender, Judith. "DNA METHYLATION AND EPIGENETICS." Annual Review of Plant Biology 55, no. 1 (June 2, 2004): 41–68. http://dx.doi.org/10.1146/annurev.arplant.55.031903.141641.

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Vanyushin, B. F. "DNA methylation and epigenetics." Russian Journal of Genetics 42, no. 9 (September 2006): 985–97. http://dx.doi.org/10.1134/s1022795406090055.

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Ly, Anna, Lesley Hoyt, Julie Crowell, and Young-In Kim. "Folate and DNA Methylation." Antioxidants & Redox Signaling 17, no. 2 (July 15, 2012): 302–26. http://dx.doi.org/10.1089/ars.2012.4554.

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47

Jones, Peter A. "DNA methylation and cancer." Oncogene 21, no. 35 (August 2002): 5358–60. http://dx.doi.org/10.1038/sj.onc.1205597.

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48

Jones, Peter A. "The DNA methylation paradox." Trends in Genetics 15, no. 1 (January 1999): 34–37. http://dx.doi.org/10.1016/s0168-9525(98)01636-9.

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Mathieu, O. "RNA-directed DNA methylation." Journal of Cell Science 117, no. 21 (October 1, 2004): 4881–88. http://dx.doi.org/10.1242/jcs.01479.

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Bonn, Dorothy. "DNA methylation and immunodeficiency." Lancet 354, no. 9191 (November 1999): 1707. http://dx.doi.org/10.1016/s0140-6736(05)76695-2.

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