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Auswahl der wissenschaftlichen Literatur zum Thema „Site-specific DNA methylation“

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Zeitschriftenartikel zum Thema "Site-specific DNA methylation"

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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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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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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4

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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5

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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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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