Methyltransferase Recruitment and DNA Hypermethylation of Target Promoters by an Oncogenic Transcription Factor

By L. Di Croce, V. Raker, M. Corsaro, F. Fazi, M. Fanelli, M. Faretta, François Fuks, F. Coco, Tony Kouzarides, C. Nervi and 2 more. Science, 2002

829 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/734797ade73ab588ed6f95c4b1615c707c5364dd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Manel Esteller
2. Peter A. Jones
3. S. Baylin
4. A. Bird
5. E. Li
6. Yi Zhang
7. R. Jaenisch
8. Anna Portela

Citations in the corpus

• Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer (2006, background): “2a ) packs the chromatin to an extent that does not allow other physiological stimuli acting on the same genes (that is, cytokines that normally trigger differentiation) to function properl”
• Establishment and Maintenance of Genomic Methylation Patterns in Mouse Embryonic Stem Cells by Dnmt3a and Dnmt3b (2003, background): “The PML-RAR fusion protein and Dnmt3L have been shown to interact with Dnmt3a and may recruit this enzyme to RAR response elements and imprinted genes, respectively (13, 18).”
• DNA methylation and cancer. (2004, background): “In one report, the leukemia-promoting PMLRAR fusion protein induced gene hypermethylation and silencing by recruiting DNA methyltransferases to target promoters.(63) Interestingly, retinoic acid treatment induced promoter demethylation, gene re-expression, and reversion of the transformed phenotype.”
• Epigenetic gene silencing in cancer: the DNA hypermethylome. (2007, background): “promyelocytic leukemia/retinoic acid receptor alpha (PML/ RARalpha), which is expressed in some leukemias, contribute to aberrant CpG-island methylation by recruiting DNMTs and HDACs to specific target genes (81), although this does not seem to be a general mechanism in this type of cancer (82).”
• Epigenetic Determinants of Cancer. (2016, background): “…enzymes, such as methyltransferases (KMTs) and demethylases (KDMs) are key for the recruitment of, or being recruited by, DNMTs, as elaborated in Figure 7 and Section 2.2.2 of Almouzni and Cedar (2014) (Di Croce et al. 2002; Fuks et al. 2003; Brenner et al. 2005; O’Hagan et al. 2011).”
• The history of cancer epigenetics (2004, neutral): “cgi?l=5914">RARα fusion protein in promyelocytic leukaemi”
• Early detection: The power and the promise of DNA methylation markers (2003, neutral): “We have also obtained some first insights into what causes DNA methylation patterns to undergo changes in cancer cell”
• Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals (2003, background): “For example, studies of unscheduled de novo methylation at the CpG island of the retinoic acid receptor-β ( RARβ”
• The fundamental role of epigenetic events in cancer (2002, background): “This methylation occurs concomitantly with the appearance of complexes that contain each of the DNMTs at the RARB promote”
• Genomic targets of the human c-Myc protein. (2003, background): “We also speculate that Myc, perhaps as an abnormal consequence of overexpression, may play a transient role in initiating DNA methylation, as shown for the chimeric oncoprotein PML-RAR (Di Croce et al. 2002).”