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En Li

Researcher at Novartis

Publications -  7
Citations -  2794

En Li is an academic researcher from Novartis. The author has contributed to research in topics: DNA methylation & RNA-Directed DNA Methylation. The author has an hindex of 6, co-authored 7 publications receiving 2649 citations. Previous affiliations of En Li include Harvard University.

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Suv39h-mediated histone H3 lysine 9 methylation directs DNA methylation to major satellite repeats at pericentric heterochromatin

TL;DR: An evolutionarily conserved pathway between histone H3-K9 methylation and DNA methylation in mammals is demonstrated and both methylation systems are likely to be important in reinforcing the stability of heterochromatic subdomains and thereby in protecting genome integrity.
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Establishment and maintenance of genomic methylation patterns in mouse embryonic stem cells by Dnmt3a and Dnmt3b.

TL;DR: It is demonstrated that genomic methylation patterns are determined partly through differential expression of different Dnmt3a and DNmt3b isoforms, and that hypermethylation of genomic DNA by Dn MT3b is necessary for ES cells to form teratomas in nude mice.
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A novel Dnmt3a isoform produced from an alternative promoter localizes to euchromatin and its expression correlates with active de novo methylation.

TL;DR: Comparison of human embryonal carcinoma cell lines with breast/ovarian cancer cell lines indicates that DNMT3A2 expression correlates with high de novo methylation activity, suggesting that Dnmt3a and DnMT3a2 may have distinct DNA targets and different functions in development.
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Complete inactivation of DNMT1 leads to mitotic catastrophe in human cancer cells

TL;DR: The results thus show that DNMT1 is required for faithfully maintaining DNA methylation patterns in human cancer cells and is essential for their proliferation and survival.
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Complete Phenotypic Characterization of apobec-1 Knockout Mice with a Wild-type Genetic Background and a Human Apolipoprotein B Transgenic Background, and Restoration of Apolipoprotein B mRNA Editing by Somatic Gene Transfer of Apobec-1

TL;DR: It is concluded that apobec-1−/− animals have a distinctive lipoprotein phenotypic effects of apoB-1 gene disruption that were not examined in the previous study, and was the cause of the elevated plasma triglyceride levels in knockout animals with a wild-type genetic background.