Literatura científica selecionada sobre o tema "Site-specific DNA methylation"
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Artigos de revistas sobre o assunto "Site-specific DNA methylation"
Choudhury, Samrat Roy, Yi Cui, Anoop Narayanan, David P. Gilley, Nazmul Huda, Chiao-Ling Lo, Feng C. Zhou, Dinesh Yernool e Joseph Irudayaraj. "Optogenetic regulation of site-specific subtelomeric DNA-methylation". Oncotarget 7, n.º 31 (4 de julho de 2016): 50380–91. http://dx.doi.org/10.18632/oncotarget.10394.
Texto completo da fonteStains, Cliff I., Jennifer L. Furman, David J. Segal e Indraneel Ghosh. "Site-Specific Detection of DNA Methylation Utilizing mCpG-SEER". Journal of the American Chemical Society 128, n.º 30 (agosto de 2006): 9761–65. http://dx.doi.org/10.1021/ja060681j.
Texto completo da fonteBruce, Sara, Katariina Hannula-Jouppi, Cecilia M. Lindgren, Marita Lipsanen-Nyman e Juha Kere. "Restriction Site–Specific Methylation Studies of Imprinted Genes with Quantitative Real-Time PCR". Clinical Chemistry 54, n.º 3 (1 de março de 2008): 491–99. http://dx.doi.org/10.1373/clinchem.2007.098491.
Texto completo da fonteNoack, Florian, Abhijeet Pataskar, Martin Schneider, Frank Buchholz, Vijay K. Tiwari e Federico Calegari. "Assessment and site-specific manipulation of DNA (hydroxy-)methylation during mouse corticogenesis". Life Science Alliance 2, n.º 2 (27 de fevereiro de 2019): e201900331. http://dx.doi.org/10.26508/lsa.201900331.
Texto completo da fonteMurata, Mariko, Ayako Takahashi, Isao Saito e Shosuke Kawanishi. "Site-specific DNA methylation and apoptosis: induction by diabetogenic streptozotocin". Biochemical Pharmacology 57, n.º 8 (abril de 1999): 881–87. http://dx.doi.org/10.1016/s0006-2952(98)00370-0.
Texto completo da fonteRajeevan, Mangalathu S., David C. Swan, Kara Duncan, Daisy R. Lee, Josef R. Limor e Elizabeth R. Unger. "Quantitation of site-specific HPV 16 DNA methylation by pyrosequencing". Journal of Virological Methods 138, n.º 1-2 (dezembro de 2006): 170–76. http://dx.doi.org/10.1016/j.jviromet.2006.08.012.
Texto completo da fonteChang, Shujun, Clint W. Magill, Jane M. Magill, Franklin Fong e Ronald J. Newton. "PCR amplification following restriction to detect site-specific DNA methylation". Plant Molecular Biology Reporter 10, n.º 4 (novembro de 1992): 362–66. http://dx.doi.org/10.1007/bf02668912.
Texto completo da fonteDong, Zizheng, Xiaofu Wang e 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, n.º 6 (1 de dezembro de 2000): G1139—G1147. http://dx.doi.org/10.1152/ajpgi.2000.279.6.g1139.
Texto completo da fonteHuang, Yung-Hsin, Su Jianzhong, Yong Lei, Michael C. Gundry, Xiaotian Zhang, Mira Jeong, Wei Li e Margaret A. Goodell. "DNA Epigenome Editing Using Crispr-Cas Suntag-Directed DNMT3A". Blood 128, n.º 22 (2 de dezembro de 2016): 2707. http://dx.doi.org/10.1182/blood.v128.22.2707.2707.
Texto completo da fonteGraessmann, A., G. Sandberg, E. Guhl e 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, n.º 3 (março de 1994): 2004–10. http://dx.doi.org/10.1128/mcb.14.3.2004-2010.1994.
Texto completo da fonteTeses / dissertações sobre o assunto "Site-specific DNA methylation"
Touzart, Aurore. "Leucémies aigüs lymphoblastiques T (LAL-T) et dérégulation épigénétique Site- and allele-specific polycomb dysregulation in T-cell leukaemia Epigenetic silencing affects L-asparaginase sensitivity and predicts outcome in T-ALL Low level CpG island promoter methylation predicts a poor outcome in adult T-ALL". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB221.
Texto completo da fonteT-ALLs are rare lymphoid neoplasms characterized by the proliferation of immature T precursors arrested at specific stages of maturation. While the genetic abnormalities involved in T-ALL leukemogenesis are becoming better known, alterations in epigenetic regulation, a very important component of the cellular homeostasis, are much less studied. My work was to tsudy the epigenetic deregulation in T-ALL through 3 main projects. In the first project, we identified an original mechanism of TAL1 oncogene deregulation. TAL1 is one of the most frequently deregulated oncogenes in T-ALL. This deregulation results mainly from translocations with the TCRδ locus or micro-deletions SIL-TAL1, two chromosomal abnormalities altering cis-regulatory elements leading to monoallelic TAL1 expression. But in a significant proportion of cases (about 50%) of TAL1+ T-ALL, an aberrant expression of TAL1 is observed without recognized mechanism suggesting unknown genetic or epigenetic mechanisms. We discovered a new somatic alteration consisting of a focal and recurrent microinsertion 7 kbp upstream of TAL1, in a non-coding intergenic region, responsible for the creation of an oncogenic "neo-enhancer" accompanied by a modification of epigenetic histone marks i.e. a “switch” from H3H27me3 repressive marks to H3K27ac activating marks. These microinsertions are a recurrent event in T-ALL and have been found in 20% of “unresolved” TAL1+ T-ALL. Through the second project, I tried to better understand the biological bases for discrepancies in patients related response to treatment. Indeed, considering two close oncogenic groups, the prognosis of TLX1+ patients, already rather favourable in the LALA-94 protocol, has not been significantly improved in the paediatric-inspired GRAALL2003-2005 trial , whereas TLX3+ patients seem to have benefited particularly from the latter; the two protocols differing mainly by L-asparaginase doses. We showed that TLX1+ patients expressed less ASNS (Asparagine synthetase) than TLX3+ and TLX- patients and that this lower expression resulted from ASNS epigenetic silencing, both by methylation of the promoter and reduction of active histone marks. A low level of ASNS methylation is also associated with lower in vitro sensitivity to L-asparaginase. Finally, ASNS methylation is an independent prognostic factor for patients included in the 2003-2005 GRAALL trial suggesting that the ASNS methylation status may be relevant for the adaptation of L-asparaginase doses. In the third project, I was interested in the global DNA methylation. MeDIP-array methylation data of a series of 24 T-ALLs allowed us to identify differential methylation signatures. We then studied the methylation status in a large series of adult T-ALL by MS-MLPA using a predictor containing 9 gene promoters. We observed that main driver oncogenes dictated methylation status. TLX1+ and TLX3+ T-ALLs displayed a hypermethylated profile and conversely, SIL-TAL1+ cases were associated with a hypomethylated profile. This methylation status is also an independent prognostic factor and hypomethylated patients have a significantly unfavorable prognosis compared to hypomethylated patients. Together, these results illustrate how disruptions in epigenetic regulation can be involved both in the T-ALL oncogenesis and in the response to treatment
Yi, Jia. "The Role of Convergent Transcription in Regulating Alternative Splicing : Targeted Epigenetic Modification via Repurposed CRISPR/Cas9 System and Its Impact on Alternative Splicing Modulation". Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS382.
Texto completo da fonteAlternative splicing of precursor RNA is a co-transcriptional process that affects the vast majority of human genes and contributes to protein diversity. Dysregulation of such process is implicated in various diseases, including tumorigenesis. However, the mechanisms regulating these processes were still to be characterized. In this study, we showed that perturbations of alternative splicing correlated with dysregulations of convergent transcription and DNA methylation. Convergent transcription could be generated between pairs of neighboring genes in opposite orientation, or between intragenic enhancers and their host gene. CENPO and ADCY3 was identified as a convergent transcription gene pair. We found, in a tumor progression model of breast cancer, that the splicing change of the ADCY3 variant exon22 correlated with an increase of its transcription that went against that of CENPO. By using targeted transcription repression system CRISPRi, we demonstrated that downregulating the transcription of CENPO could not reverse the alternative splicing alteration of ADCY3 in cancer cells (DCIS). An active intragenic enhancer was identified in the intron16 of CD44, at the downstream of its alternative exons. By using targeted transcription activation system CRISPRa, we showed that upregulating the transcription of CD44 could not alter the alternative splicing of CD44 in DCIS cells. These results suggest that convergent transcription modulation through changes of promoter activity does not alter the alternative splicing of ADCY3 and CD44 in DCIS cells. However, through replacing the intragenic enhancer by an inducible promoter, we found that intragenic transcription activation increased the inclusion level of several alternative exons of CD44 in HCT116 cells. This result suggested that local convergent transcription could have a direct impact on the alternative splicing of CD44. Furthermore, by using targeted DNA methylation system CRISPR/dCas9-DNMT3b, we showed that DNA methylation at variant exons could directly modify CD44 alternative splicing. This thesis work also explored the limitation and feasibility of studying alternative splicing with repurposed CRISPR systems
Smith, Lacie Marie. "Synthesis of site specific DNA methylating compounds targeting pancreatic ß-cells". View electronic thesis, 2008. http://dl.uncw.edu/etd/2008-3/smithl/laciesmith.pdf.
Texto completo da fonteLivros sobre o assunto "Site-specific DNA methylation"
Stempak, Joanne Mary. The effects of folate deficiency on genomic and site-specific DNA methylation. Ottawa: National Library of Canada, 2003.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Site-specific DNA methylation"
Nelson, Michael, Yanping Zhang e James L. Etten. "DNA methyltransferases and DNA site-specific endonucleases encoded by chlorella viruses". In DNA Methylation, 186–211. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_9.
Texto completo da fonteKaminsky, Zachary, e Arturas Petronis. "Methylation SNaPshot: A Method for the Quantification of Site-Specific DNA Methylation Levels". In Methods in Molecular Biology, 241–55. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-522-0_18.
Texto completo da fonte