Cancer-associated DNA hypermethylation of Polycomb targets requires DNMT3A dual recognition of histone H2AK119 ubiquitination and the nucleosome acidic patch

During tumor development, promoter CpG islands that are normally silenced by Polycomb repressive complexes (PRCs) become DNA-hypermethylated. The molecular mechanism by which de novo DNA methyltransferase(s) [DNMT(s)] catalyze CpG methylation at PRC-regulated regions remains unclear. Here, we report...

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Veröffentlicht in:	Science advances 2024-08, Vol.10 (35), p.eadp0975
Hauptverfasser:	Gretarsson, Kristjan H, Abini-Agbomson, Stephen, Gloor, Susan L, Weinberg, Daniel N, McCuiston, Jamie L, Kumary, Vishnu Udayakumar Sunitha, Hickman, Allison R, Sahu, Varun, Lee, Rachel, Xu, Xinjing, Lipieta, Natalie, Flashner, Samuel, Adeleke, Oluwatobi A, Popova, Irina K, Taylor, Hailey F, Noll, Kelsey, Windham, Carolina Lin, Maryanski, Danielle N, Venters, Bryan J, Nakagawa, Hiroshi, Keogh, Michael-Christopher, Armache, Karim-Jean, Lu, Chao
Format:	Artikel
Sprache:	eng
Schlagworte:	Biomedicine and Life Sciences Cancer Cell Line, Tumor CpG Islands Cryoelectron Microscopy DNA (Cytosine-5-)-Methyltransferases - genetics DNA (Cytosine-5-)-Methyltransferases - metabolism DNA Methylation DNA Methyltransferase 3A Histones - metabolism Humans Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Nucleosomes - metabolism Polycomb-Group Proteins - genetics Polycomb-Group Proteins - metabolism Promoter Regions, Genetic Protein Binding SciAdv r-articles Structural Biology Ubiquitination
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