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oai:repisalud.isciii.es:20.500.12105/179682024-11-29T14:15:12Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Espada, Jesús author Peinado, Hector author Lopez-Serra, Lidia author Setién, Fernando author Lopez-Serra, Paula author Portela, Anna author Renart, Jaime author Carrasco, Elisa author Calvo, María author Juarranz, Angeles author Cano, Amparo author Esteller, Manel author 2011-11 Mammalian DNA methyltransferase 1 (DNMT1) is essential for maintaining DNA methylation patterns after cell division. Disruption of DNMT1 catalytic activity results in whole genome cytosine demethylation of CpG dinucleotides, promoting severe dysfunctions in somatic cells and during embryonic development. While these observations indicate that DNMT1-dependent DNA methylation is required for proper cell function, the possibility that DNMT1 has a role independent of its catalytic activity is a matter of controversy. Here, we provide evidence that DNMT1 can support cell functions that do not require the C-terminal catalytic domain. We report that PCNA and DMAP1 domains in the N-terminal region of DNMT1 are sufficient to modulate E-cadherin expression in the absence of noticeable changes in DNA methylation patterns in the gene promoters involved. Changes in E-cadherin expression are directly associated with regulation of β-catenin-dependent transcription. Present evidence suggests that the DNMT1 acts on E-cadherin expression through its direct interaction with the E-cadherin transcriptional repressor SNAIL1. Nucleic Acids Res . 2011;39(21):9194-205 10.1093/nar/gkr658 1362-4962 Nucleic acids research https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241660/pdf/gkr658.pdf 21846773 http://hdl.handle.net/20.500.12105/17968 Regulation of SNAIL1 and E-cadherin function by DNMT1 in a DNA methylation-independent context.