dc.creatorArratia, Felipe
dc.creatorFierro, Cristopher
dc.creatorBlanco, Alejandro
dc.creatorFuentes, Sebastián
dc.creatorNahuelquen, Daniela
dc.creatorMontecino, Martin
dc.creatorRojas, Adriana
dc.creatorAguilar, Rodrigo
dc.date.accessioned2023-12-05T18:56:43Z
dc.date.accessioned2024-05-02T15:09:07Z
dc.date.available2023-12-05T18:56:43Z
dc.date.available2024-05-02T15:09:07Z
dc.date.created2023-12-05T18:56:43Z
dc.date.issued2023-06
dc.identifierCurrent Issues in Molecular Biology Open Access Volume 45, Issue 6, Pages 4735 - 4748June 2023
dc.identifier14673037
dc.identifierhttps://repositorio.unab.cl/xmlui/handle/ria/54415
dc.identifier10.3390/cimb45060301
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/9263288
dc.description.abstractIn cancer cells, the long non-coding RNA (lncRNA) MALAT1 has arisen as a key partner for the Polycomb Repressive Complex 2 (PRC2), an epigenetic modifier. However, it is unknown whether this partnership occurs genome-wide at the chromatin level, as most of the studies focus on single genes that are usually repressed. Due to the genomic binding properties of both macromolecules, we wondered whether there are binding sites shared by PRC2 and MALAT1. Using public genome-binding datasets for PRC2 and MALAT1 derived from independent ChIP- and CHART-seq experiments performed with the breast cancer cell line MCF7, we searched for regions containing PRC2 and MALAT1 overlapping peaks. Peak calls for each molecule were performed using MACS2 and then overlapping peaks were identified by bedtools intersect. Using this approach, we identified 1293 genomic sites where PRC2 and MALAT1 concur. Interestingly, 54.75% of those sites are within gene promoter regions ([removed]
dc.languageen
dc.publisherMDPI
dc.rightshttps://creativecommons.org/licenses/by/4.0/
dc.rightsCC BY 4.0 DEED
dc.subjectChromatin
dc.subjectLong non-coding RNA
dc.subjectMALAT1
dc.subjectPolycomb Repressive Complex 2
dc.titleSelective Concurrence of the Long Non-Coding RNA MALAT1 and the Polycomb Repressive Complex 2 to Promoter Regions of Active Genes in MCF7 Breast Cancer Cells
dc.typeArtículo


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