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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The methylome of Alu repeats in colon cancer (CGH)

ABSTRACT: Next Generation Sequencing of Unmethylated Alu (NSUMA) interrogation of more than 130,000 individual Alus for differential methylation with concomitant analysis of copy number variations applied to the study of hypomethylation in colorectal cancer. normal colon tissues, matched primary tumors, and colon derived cell lines

ORGANISM(S): Homo sapiens

SUBMITTER: Miguel Peinado

PROVIDER: E-GEOD-72750 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The methylome of Alu repeats in colon cancer (NSUMA)

Project description:Next Generation Sequencing of Unmethylated Alu (NSUMA) interrogation of more than 130,000 individual Alus for differential methylation with concomitant analysis of copy number variations applied to the study of hypomethylation in colorectal cancer. normal colon tissues, matched primary tumors, blood and colon derived cell lines

2015-09-08 | E-GEOD-72749 | biostudies-arrayexpress

The methylome of Alu repeats in primates

2015-09-10 | GSE72877 | GEO

The methylome of Alu repeats in primates

Project description:Next Generation Sequencing of Unmethylated Alu (NSUMA) interrogation of more than 130,000 individual Alus for differential methylation with concomitant analysis of copy number variations applied to the study of hypomethylation in primates. 3 replicates of Gorilla gorilla, Pan troglodytes, Pongo pygmaeus and Homo sapiens were studied.

2015-09-10 | E-GEOD-72877 | biostudies-arrayexpress

The methylome of Alu repeats in colon cancer (NSUMA)

2015-09-08 | GSE72749 | GEO

The methylome of Alu repeats in colon cancer (CGH)

2015-09-08 | GSE72750 | GEO

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Verification of predicted hotspots of Alu/Alu-mediated rearrangements in the human genome

Project description:To identify the genome-wide impact of Alu/Alu-mediated rearrangement (AAMR) on variation and human health, we have developed a bioinformatic approach to characterize Alus involved in mediating CNVs and have predicted genome-wide AAMR hotspot loci. This prediction was validated by performing molecular biological experiments on 89 samples selected by correlating AAMR hotspot genes with a database of ~54,000 chromosomal microarrays.

2017-06-29 | GSE100590 | GEO

The methylome of Alu repeats in colon cancer

Project description:The methylome of Alu repeats in colon cancer

| PRJNA294809 | ENA

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

Project description:Alu retrotransposons, forming the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their bulk expression has long been known to increase in response to various types of stress, including viral infection. Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus, by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase and of the YAP1 and FOS transcription factors. The physical interaction of e1a with the chromatin remodeler EP400 turned out to be critical for Alu derepression, and upstream enrichment of EP400 was found to commonly demarcate expression-prone Alus. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, mediated by e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenovirus.

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Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

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