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Thematische Bibliographien / Site-specific DNA methylation / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Site-specific DNA methylation“

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Veröffentlicht am 25. Mai 2024

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1

Choudhury, Samrat Roy, Yi Cui, Anoop Narayanan, et al. "Optogenetic regulation of site-specific subtelomeric DNA-methylation." Oncotarget 7, no. 31 (2016): 50380–91. http://dx.doi.org/10.18632/oncotarget.10394.

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2

Stains, Cliff I., Jennifer L. Furman, David J. Segal, and Indraneel Ghosh. "Site-Specific Detection of DNA Methylation Utilizing mCpG-SEER." Journal of the American Chemical Society 128, no. 30 (2006): 9761–65. http://dx.doi.org/10.1021/ja060681j.

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3

Bruce, Sara, Katariina Hannula-Jouppi, Cecilia M. Lindgren, Marita Lipsanen-Nyman, and Juha Kere. "Restriction Site–Specific Methylation Studies of Imprinted Genes with Quantitative Real-Time PCR." Clinical Chemistry 54, no. 3 (2008): 491–99. http://dx.doi.org/10.1373/clinchem.2007.098491.

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Abstract Background: Epigenetic studies, such as the measurement of DNA methylation, are important in the investigation of syndromes influenced by imprinted genes. Quick and accurate quantification of methylation at such genes can be of appreciable diagnostic aid. Methods: We first digested genomic DNA with methylation-sensitive restriction enzymes and used DNA without digestion as a control and nonmethylated λ DNA as an internal control for digestion efficiency. We then performed quantitative real-time PCR analyses with 6 unique PCR assays to investigate 4 imprinting control regions on chromo

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Noack, Florian, Abhijeet Pataskar, Martin Schneider, Frank Buchholz, Vijay K. Tiwari, and Federico Calegari. "Assessment and site-specific manipulation of DNA (hydroxy-)methylation during mouse corticogenesis." Life Science Alliance 2, no. 2 (2019): e201900331. http://dx.doi.org/10.26508/lsa.201900331.

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Dynamic changes in DNA (hydroxy-)methylation are fundamental for stem cell differentiation. However, the signature of these epigenetic marks in specific cell types during corticogenesis is unknown. Moreover, site-specific manipulation of cytosine modifications is needed to reveal the significance and function of these changes. Here, we report the first assessment of (hydroxy-)methylation in neural stem cells, neurogenic progenitors, and newborn neurons during mammalian corticogenesis. We found that gain in hydroxymethylation and loss in methylation occur sequentially at specific cellular trans

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Murata, Mariko, Ayako Takahashi, Isao Saito, and Shosuke Kawanishi. "Site-specific DNA methylation and apoptosis: induction by diabetogenic streptozotocin." Biochemical Pharmacology 57, no. 8 (1999): 881–87. http://dx.doi.org/10.1016/s0006-2952(98)00370-0.

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6

Rajeevan, Mangalathu S., David C. Swan, Kara Duncan, Daisy R. Lee, Josef R. Limor, and Elizabeth R. Unger. "Quantitation of site-specific HPV 16 DNA methylation by pyrosequencing." Journal of Virological Methods 138, no. 1-2 (2006): 170–76. http://dx.doi.org/10.1016/j.jviromet.2006.08.012.

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7

Chang, Shujun, Clint W. Magill, Jane M. Magill, Franklin Fong, and Ronald J. Newton. "PCR amplification following restriction to detect site-specific DNA methylation." Plant Molecular Biology Reporter 10, no. 4 (1992): 362–66. http://dx.doi.org/10.1007/bf02668912.

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8

Dong, Zizheng, Xiaofu Wang, and B. Mark Evers. "Site-specific DNA methylation contributes to neurotensin/neuromedin N expression in colon cancers." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 6 (2000): G1139—G1147. http://dx.doi.org/10.1152/ajpgi.2000.279.6.g1139.

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The neurotensin/neuromedin N (NT/N) gene is expressed in fetal colon, repressed in newborn and adult colon, and reexpressed in ∼25% of colon cancers. Our purpose was to determine the effect of gene methylation on NT/N silencing in colon cancers. We found that the NT/N gene was expressed in human colon cancer cell line KM12C but not in KM20 colon cancer cells. Bisulfite genomic sequencing demonstrated that all CpG dinucleotides in the region from −373 to +100 of the NT/N promoter, including a CpG site in a distal consensus AP-1 site, were methylated in KM20 but unmethylated in KM12C cells. Trea

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Huang, Yung-Hsin, Su Jianzhong, Yong Lei, et al. "DNA Epigenome Editing Using Crispr-Cas Suntag-Directed DNMT3A." Blood 128, no. 22 (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 sit

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Graessmann, A., G. Sandberg, E. Guhl, and M. Graessmann. "Methylation of single sites within the herpes simplex virus tk coding region and the simian virus 40 T-antigen intron causes gene inactivation." Molecular and Cellular Biology 14, no. 3 (1994): 2004–10. http://dx.doi.org/10.1128/mcb.14.3.2004-2010.1994.

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In order to determine whether partial methylation of the herpes simplex virus (HSV) tk gene prevents tk gene expression, the HSV tk gene was cloned as single-stranded DNA. By in vitro second-strand DNA synthesis, specific HSV tk gene segments were methylated, and the hemimethylated DNA molecules were microinjected into thymidine kinase-negative rat2 cells. Conversion of the hemimethylated DNA into symmetrical methylated DNA and integration into the host genome occurred early after gene transfer, before the cells entered into the S phase. HSV tk gene expression was inhibited either by promoter

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Graessmann, A., G. Sandberg, E. Guhl, and M. Graessmann. "Methylation of single sites within the herpes simplex virus tk coding region and the simian virus 40 T-antigen intron causes gene inactivation." Molecular and Cellular Biology 14, no. 3 (1994): 2004–10. http://dx.doi.org/10.1128/mcb.14.3.2004.

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In order to determine whether partial methylation of the herpes simplex virus (HSV) tk gene prevents tk gene expression, the HSV tk gene was cloned as single-stranded DNA. By in vitro second-strand DNA synthesis, specific HSV tk gene segments were methylated, and the hemimethylated DNA molecules were microinjected into thymidine kinase-negative rat2 cells. Conversion of the hemimethylated DNA into symmetrical methylated DNA and integration into the host genome occurred early after gene transfer, before the cells entered into the S phase. HSV tk gene expression was inhibited either by promoter

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Grant, DJ, H. Shi, and CT Teng. "Tissue and site-specific methylation correlates with expression of the mouse lactoferrin gene." Journal of Molecular Endocrinology 23, no. 1 (1999): 45–55. http://dx.doi.org/10.1677/jme.0.0230045.

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We have previously examined the regulatory region of the mouse lactoferrin gene and have identified sequences essential for basal and hormonally induced expression. In this study, we explore the relationship between the methylation state of the mouse lactoferrin gene promoter and its expression in selected mouse tissues. In a transient expression system, transcriptional activity was blocked after in vitro methylation of the regulatory region of the mouse lactoferrin gene. In addition, the in vivo methylation state of three promoter region sites was assessed using Southern blot analysis of DNA

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ZHANG, ZHI-XIN, VIPIN KUMAR, RAY T. RIVERA, SALLY G. PASION, JANE CHISHOLM, and DEBAJIT K. BISWAS. "Suppression of Prolactin Gene Expression in GH Cells Correlates with Site-Specific DNA Methylation." DNA 8, no. 8 (1989): 605–13. http://dx.doi.org/10.1089/dna.1989.8.605.

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Nomura, Wataru, and Carlos F. Barbas. "In Vivo Site-Specific DNA Methylation with a Designed Sequence-Enabled DNA Methylase." Journal of the American Chemical Society 129, no. 28 (2007): 8676–77. http://dx.doi.org/10.1021/ja0705588.

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Tirosh, Amit, Jonathan Keith Killian, David Petersen, et al. "Distinct DNA Methylation Signatures in Neuroendocrine Tumors Specific for Primary Site and Inherited Predisposition." Journal of Clinical Endocrinology & Metabolism 105, no. 10 (2020): 3285–94. http://dx.doi.org/10.1210/clinem/dgaa477.

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Abstract Purpose To compare the deoxyribonucleic acid (DNA) methylation signature of neuroendocrine tumors (NETs) by primary tumor site and inherited predisposition syndromes von Hippel–Lindau disease (VHL) and multiple endocrine neoplasia type 1 (MEN1). Methods Genome-wide DNA methylation (835 424 CpGs) of 96 NET samples. Principal components analysis (PCA) and unsupervised hierarchical clustering analyses were used to determine DNA methylome signatures. Results Hypomethylated CpGs were significantly more common in VHL-related versus sporadic and MEN1-related NETs (P &lt; .001 for both co

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Rao, B. S., and A. Buckler-White. "Direct visualization of site-specific and strand-specific DNA methylation patterns in automated DNA sequencing data." Nucleic Acids Research 26, no. 10 (1998): 2505–7. http://dx.doi.org/10.1093/nar/26.10.2505.

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Han, Weiguo, Miao Shi, and Simon D. Spivack. "Site-specific methylated reporter constructs for functional analysis of DNA methylation." Epigenetics 8, no. 11 (2013): 1176–87. http://dx.doi.org/10.4161/epi.26195.

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McDonald, James I., Hamza Celik, Lisa E. Rois, et al. "Reprogrammable CRISPR/Cas9-based system for inducing site-specific DNA methylation." Biology Open 5, no. 6 (2016): 866–74. http://dx.doi.org/10.1242/bio.019067.

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Nelson, M., and M. McClelland. "Site-specific methylation: effect on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 19, suppl (1991): 2045–71. http://dx.doi.org/10.1093/nar/19.suppl.2045.

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Healey, Matthew J., William Rowe, Sofia Siati, Muttuswamy Sivakumaran, and Mark Platt. "Rapid Assessment of Site Specific DNA Methylation through Resistive Pulse Sensing." ACS Sensors 3, no. 3 (2018): 655–60. http://dx.doi.org/10.1021/acssensors.7b00935.

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Blattler, Adam, and Peggy J. Farnham. "Cross-talk between Site-specific Transcription Factors and DNA Methylation States." Journal of Biological Chemistry 288, no. 48 (2013): 34287–94. http://dx.doi.org/10.1074/jbc.r113.512517.

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Ogushi, Shoko, Yuya Yoshida, Tsuyoshi Nakanishi, and Tomoki Kimura. "CpG Site-Specific Regulation of Metallothionein-1 Gene Expression." International Journal of Molecular Sciences 21, no. 17 (2020): 5946. http://dx.doi.org/10.3390/ijms21175946.

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Metal-binding inducible proteins called metallothioneins (MTs) protect cells from heavy-metal toxicity. Their transcription is regulated by metal response element (MRE)-binding transcription factor-1 (MTF1), which is strongly recruited to MREs in the MT promoters, in response to Zn and Cd. Mouse Mt1 gene promoter contains 5 MREs (a–e), and MTF1 has the highest affinity to MREd. Epigenetic changes like DNA methylation might affect transcription and, therefore, the cytoprotective function of MT genes. To reveal the CpG site(s) critical for Mt1 transcription, we analyzed the methylation status of

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Bernstein, Carol. "DNA Methylation and Establishing Memory." Epigenetics Insights 15 (January 2022): 251686572110724. http://dx.doi.org/10.1177/25168657211072499.

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A single event can cause a life-long memory. Memories physically reside in neurons, and changes in neuronal gene expression are considered to be central to memory. Early models proposed that specific DNA methylations of cytosines in neuronal DNA encode memories in a stable biochemical form. This review describes recent research that elucidates the molecular mechanisms used by the mammalian brain to form DNA methylcytosine encoded memories. For example, neuron activation initiates cytosine demethylation by stimulating DNA topoisomerase II beta (TOP2B) protein to make a temporary DNA double-stra

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Lu, Qianjin, Donna Ray, David Gutsch, and Bruce Richardson. "Effect of DNA methylation and chromatin structure onITGAL expression." Blood 99, no. 12 (2002): 4503–8. http://dx.doi.org/10.1182/blood.v99.12.4503.

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LFA-1 (CD11a/CD18, αLβ2) is an integrin expressed in a tissue-specific fashion and is important in inflammatory and immune responses. Promoter analysis has identified transcription factors that may be involved in CD11a expression, but the mechanisms contributing to its tissue-specific expression are incompletely characterized. In this report we have asked if DNA methylation and/or chromatin structure could contribute to tissue-specific CD11a expression. Bisulfite sequencing was used to compare methylation patterns in the promoter and 5′ flanking regions of the ITGAL gene, encoding CD11a, in no

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Wang, Heng, Yumo Xie, Gaopo Xu, et al. "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 (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 t

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McClelland, M., and M. Nelson. "Effect of site-specific methylation on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 20, suppl (1992): 2145–57. http://dx.doi.org/10.1093/nar/20.suppl.2145.

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Nelson, Michael, Eberhard Raschke, and Michael McClelland. "Effect of site-specific methylation on restriction endonucleases and DNA modification methyltransferases." Nucleic Acids Research 21, no. 13 (1993): 3139–54. http://dx.doi.org/10.1093/nar/21.13.3139.

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Narasimhan, Supraja, Virginia R. Falkenberg, Maung M. Khin, and Mangalathu S. Rajeevan. "Determination of quantitative and site-specific DNA methylation of perforin by pyrosequencing." BMC Research Notes 2, no. 1 (2009): 104. http://dx.doi.org/10.1186/1756-0500-2-104.

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Wen, Hui, Hui Wang, Honghong Wang, Jingli Yan, Hui Tian, and Zhengping Li. "Ultrasensitive detection of site-specific DNA methylation by loop-mediated isothermal amplification." Anal. Methods 8, no. 27 (2016): 5372–77. http://dx.doi.org/10.1039/c6ay00999a.

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Nelson, M., and M. McClelland. "Effect of site-specific methylation on DNA modification methyltransferases and restriction endonucleases." Nucleic Acids Research 17, suppl (1989): r389—r415. http://dx.doi.org/10.1093/nar/17.suppl.r389.

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Kishton, Rigel J., Sean E. Miller, Heather Perry, et al. "DNA site-specific N3-adenine methylation targeted to estrogen receptor-positive cells." Bioorganic & Medicinal Chemistry 19, no. 17 (2011): 5093–102. http://dx.doi.org/10.1016/j.bmc.2011.07.026.

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Gaido, M. L., and J. S. Strobl. "Inhibition of rat growth hormone promoter activity by site-specific DNA methylation." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1008, no. 2 (1989): 234–42. http://dx.doi.org/10.1016/0167-4781(80)90014-7.

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Genereux, D. P., B. E. Miner, C. T. Bergstrom, and C. D. Laird. "A population-epigenetic model to infer site-specific methylation rates from double-stranded DNA methylation patterns." Proceedings of the National Academy of Sciences 102, no. 16 (2005): 5802–7. http://dx.doi.org/10.1073/pnas.0502036102.

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Caspers, Maarten, Sara Blocquiaux, Ruben Charlier, et al. "Intensity-Specific Differential Leukocyte DNA Methylation in Physical (In)Activity: An Exploratory Approach." Twin Research and Human Genetics 21, no. 2 (2018): 101–11. http://dx.doi.org/10.1017/thg.2018.10.

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The aim of this exploratory study was to investigate how sedentary behavior (SB) and physical activity (PA) influence DNA methylation at a global, gene-specific, and health-related pathway level. SB, light PA (LPA), and moderate-to-vigorous PA (MVPA) were assessed objectively for 41 Flemish men using the SenseWear Pro 3 Armband. CpG site-specific methylation in leukocytes was determined using the Illumina HumanMethylation 450 BeadChip. Correlations were calculated between time spent on the three PA intensity levels and global DNA methylation, using a z-score-based method to determine global DN

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van der Woude, Marjan, W. Bradley Hale, and David A. Low. "Formation of DNA Methylation Patterns: Nonmethylated GATC Sequences in gut and papOperons." Journal of Bacteriology 180, no. 22 (1998): 5913–20. http://dx.doi.org/10.1128/jb.180.22.5913-5920.1998.

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ABSTRACT Most of the adenine residues in GATC sequences in theEscherichia coli chromosome are methylated by the enzyme deoxyadenosine methyltransferase (Dam). However, at least 20 GATC sequences remain nonmethylated throughout the cell cycle. Here we examined how the DNA methylation patterns of GATC sequences within the regulatory regions of the pyelonephritis-associated pilus (pap) operon and the glucitol utilization (gut) operon were formed. The results obtained with an in vitro methylation protection assay showed that the addition of the leucine-responsive regulatory protein (Lrp) to pap DN

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Małodobra-Mazur, Małgorzata, Aneta Cierzniak, Krzysztof Kaliszewski, and Tadeusz Dobosz. "PPARG Hypermethylation as the First Epigenetic Modification in Newly Onset Insulin Resistance in Human Adipocytes." Genes 12, no. 6 (2021): 889. http://dx.doi.org/10.3390/genes12060889.

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Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Insulin resistance (IR) is a state when the physiological amount of insulin is not sufficient to evoke proper action, i.e., glucose uptake. Epigenetic modifications associated with obesity and IR are some of the main mechanisms leading to IR pathogenesis. The mesenchymal stem cells of adipose tissue (subcutaneous (SAT) and visceral (VAT)) were collected during abdominal surgery. IR was induced ex vivo by palmitic acid. DNA methylation was determi

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Mullins, L. J., G. Veres, C. T. Caskey, and V. Chapman. "Differential methylation of the ornithine carbamoyl transferase gene on active and inactive mouse X chromosomes." Molecular and Cellular Biology 7, no. 11 (1987): 3916–22. http://dx.doi.org/10.1128/mcb.7.11.3916-3922.1987.

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Ornithine carbamoyl transferase (Oct) is an X-linked gene which exhibits tissue-specific expression. To determine whether methylation of specific CpG sequences plays a role in dosage compensation or tissue-specific expression of the gene, 13 potentially methylatable sites were identified over a 30-kilobase (kb) region spanning from approximately 15 kb upstream to beyond exon II. Fragments of the Mus hortulanus Oct gene were used as probes to establish the degree of methylation at each site. By considering the methylation status in liver (expressing tissue) versus kidney (nonexpressing tissue)

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Mullins, L. J., G. Veres, C. T. Caskey, and V. Chapman. "Differential methylation of the ornithine carbamoyl transferase gene on active and inactive mouse X chromosomes." Molecular and Cellular Biology 7, no. 11 (1987): 3916–22. http://dx.doi.org/10.1128/mcb.7.11.3916.

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Ornithine carbamoyl transferase (Oct) is an X-linked gene which exhibits tissue-specific expression. To determine whether methylation of specific CpG sequences plays a role in dosage compensation or tissue-specific expression of the gene, 13 potentially methylatable sites were identified over a 30-kilobase (kb) region spanning from approximately 15 kb upstream to beyond exon II. Fragments of the Mus hortulanus Oct gene were used as probes to establish the degree of methylation at each site. By considering the methylation status in liver (expressing tissue) versus kidney (nonexpressing tissue)

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Lavender, P., A. J. L. Clark, G. M. Besser, and L. H. Rees. "Variable methylation of the 5′-flanking DNA of the human pro-opiomelanocortin gene." Journal of Molecular Endocrinology 6, no. 1 (1991): 53–61. http://dx.doi.org/10.1677/jme.0.0060053.

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ABSTRACT The pro-opiomelanocortin gene is widely expressed in human tissues, although both transcriptional initiation sites and regulation appear to be tissue specific. In order to determine how promoter and enhancer choice is effected, we have studied the methylation pattern of the gene in a number of normal tissues, tumours and cell lines. Variability of this pattern was observed in the 5′-flanking DNA, particularly at the HpaII site located at −304 bp upstream from the pituitary CAP site. This site was generally methylated in tissues likely to express the predominant extrapituitary (800 nuc

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Ling, Li, Meng Ren, Chuan Yang та ін. "Role of site-specific DNA demethylation in TNFα-induced MMP9 expression in keratinocytes". Journal of Molecular Endocrinology 50, № 3 (2013): 279–90. http://dx.doi.org/10.1530/jme-12-0172.

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Inappropriately high expression of matrix metalloproteinase 9 (MMP9) in the late stage of diabetic foot ulcers suppresses wound healing. The underlying mechanisms are not completely understood. Site-specific demethylation was reported to function in the regulation of genes, causing persistent high expression of target genes. Therefore, this study was designed to determine whether site-specific DNA demethylation was a key regulatory component ofMMP9expression in diabetic wound healing, and to further verify the crucial CpG site(s). Human keratinocyte cell line (HaCaT) cells were exposed to tumo

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Li, Shufen, Zhongju Wang, Lin Zhou, Fu Luo, and Cunyou Zhao. "Fluorescence polarization-based method with bisulfite conversion-specific one-label extension for quantification of single CpG dinucleotide methylation." Genome 58, no. 7 (2015): 357–63. http://dx.doi.org/10.1139/gen-2014-0185.

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To quantify the methylation at individual CpG dinucleotide sites in large biological or clinical samples, we developed a bisulfite conversion-specific one-label extension (BS-OLE) method using visualization by fluorescence polarization (FP) measurement of methylation at single CpG sites in small amounts of genomic DNA. Genomic DNA was treated with sodium bisulfite to convert unmethylated cytosine to uracil leaving 5-methylcytosine unaltered, and BS-PCR was used to generate DNA template containing target CpG sites. BS-OLE uses a BS-primer hybridized immediately upstream of the target CpG site b

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Umezawa, A., H. Yamamoto, K. Rhodes, M. J. Klemsz, R. A. Maki, and R. G. Oshima. "Methylation of an ETS site in the intron enhancer of the keratin 18 gene participates in tissue-specific repression." Molecular and Cellular Biology 17, no. 9 (1997): 4885–94. http://dx.doi.org/10.1128/mcb.17.9.4885.

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The activities of ETS transcription factors are modulated by posttranscriptional modifications and cooperation with other proteins. Another factor which could alter the regulation of genes by ETS transcription factors is DNA methylation of their cognate binding sites. The optimal activity of the keratin 18 (K18) gene is dependent upon an ETS binding site within an enhancer region located in the first intron. The methylation of the ETS binding site was correlated with the repression of the K18 gene in normal human tissues and in K18 transgenic mouse tissues. Neither recombinant ETS2 nor endogen

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Spainhour, John CG, Hong Seo Lim, Soojin V. Yi, and Peng Qiu. "Correlation Patterns Between DNA Methylation and Gene Expression in The Cancer Genome Atlas." Cancer Informatics 18 (January 2019): 117693511982877. http://dx.doi.org/10.1177/1176935119828776.

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Background: DNA methylation is a form of epigenetic modification that has been shown to play a significant role in gene regulation. In cancer, DNA methylation plays an important role by regulating the expression of oncogenes. The role of DNA methylation in the onset and progression of various cancer types is now being elucidated as more large-scale data become available. The Cancer Genome Atlas (TCGA) provides a wealth of information for the analysis of various molecular aspects of cancer genetics. Gene expression data and DNA methylation data from TCGA have been used for a variety of studies.

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Dukatz, Michael, Sabrina Adam, Mahamaya Biswal, Jikui Song, Pavel Bashtrykov, and Albert Jeltsch. "Complex DNA sequence readout mechanisms of the DNMT3B DNA methyltransferase." Nucleic Acids Research 48, no. 20 (2020): 11495–509. http://dx.doi.org/10.1093/nar/gkaa938.

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Abstract DNA methyltransferases interact with their CpG target sites in the context of variable flanking sequences. We investigated DNA methylation by the human DNMT3B catalytic domain using substrate pools containing CpX target sites in randomized flanking context and identified combined effects of CpG recognition and flanking sequence interaction together with complex contact networks involved in balancing the interaction with different flanking sites. DNA methylation rates were more affected by flanking sequences at non-CpG than at CpG sites. We show that T775 has an essential dynamic role

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Xu, Jian-Hong, Ruixian Wang, Xinxin Li, Mihai Miclaus, and Joachim Messing. "Locus- and Site-Specific DNA Methylation of 19 kDa Zein Genes in Maize." PLOS ONE 11, no. 1 (2016): e0146416. http://dx.doi.org/10.1371/journal.pone.0146416.

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Suzuki, M., T. Yamada, F. Kihara-Negishi, et al. "Site-specific DNA methylation by a complex of PU.1 and Dnmt3a/b." Oncogene 25, no. 17 (2005): 2477–88. http://dx.doi.org/10.1038/sj.onc.1209272.

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McClelland, Michael, and Michael Nelson. "The effect of site-specific DNA methylation on restriction endonucleases and DNA modification methyltransferases — a review." Gene 74, no. 1 (1988): 291–304. http://dx.doi.org/10.1016/0378-1119(88)90305-8.

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Peshavaria, M., and I. N. M. Day. "Methylation patterns in the human muscle-specific enolase gene (ENO3)." Biochemical Journal 292, no. 3 (1993): 701–4. http://dx.doi.org/10.1042/bj2920701.

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The methylation status in the human-muscle enolase gene (ENO3) was assayed. Previous sequence data and MspI cleavage sites indicate the presence of a 5′ CpG-rich island of at least 4 kb: none of 22 characterized MspI CCGG sites is methylated in any of muscle, sperm or brain DNA. However a complex pattern of complete and partial methylation of MspI sites that is different between tissues is observed within the ENO3 gene: events at one site may be specific to muscle DNA. The absence of methylation in the promoter region of the ENO3 gene makes it unlikely that methylation plays a causal role eith

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Xie, Xuemei, Hongjie Gao, Wanjiang Zeng та ін. "Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level". Clinical Science 129, № 4 (2015): 385–94. http://dx.doi.org/10.1042/cs20140688.

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Among all the participants, the maternal gestational glucose level was positively correlated with placental DNA methylation. The correlation between gestational 2-h post-OGTT glycaemia and CpG site-specific methylation in placenta was stronger in the gestational diabetes group.

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Patil, Vibha, Cyrille Cuenin, Felicia Chung, et al. "Human mitochondrial DNA is extensively methylated in a non-CpG context." Nucleic Acids Research 47, no. 19 (2019): 10072–85. http://dx.doi.org/10.1093/nar/gkz762.

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Abstract Mitochondrial dysfunction plays critical roles in cancer development and related therapeutic response; however, exact molecular mechanisms remain unclear. Recently, alongside the discovery of mitochondrial-specific DNA methyltransferases, global and site-specific methylation of the mitochondrial genome has been described. Investigation of any functional consequences however remains unclear and debated due to insufficient evidence of the quantitative degree and frequency of mitochondrial DNA (mtDNA) methylation. This study uses WGBS to provide the first quantitative report of mtDNA met

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