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Genome-wide mapping of 8-oxodG and gH2AX in growing MCF10A cells and MEFs

ABSTRACT: Genome-wide mapping of 8-oxodG and gH2AX in growing MCF10A cells and MEFs

PROVIDER: PRJNA391133 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5714924.fastq.gz	Fastqsanger.gz
	SRR5714925.fastq.gz	Fastqsanger.gz
	SRR5714926.fastq.gz	Fastqsanger.gz
	SRR5714927.fastq.gz	Fastqsanger.gz
	SRR5714928.fastq.gz	Fastqsanger.gz

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Genome-wide mapping of 8-oxodG and gH2AX in growing MCF10A cells and MEFs

Project description:8-oxo-7,8-dihydro-2’-deoxyguanine (8-oxodG) is one of the major DNA modifications and a potent pre-mutagenic lesion prone to mispair with deoxyadenine (dA). Several thousand residues of 8-oxodG spread constitutively in the genome of human cells, but their genomic distribution has not yet been characterized. Here, by using OxyDIP-Seq, a highly sensitive methodology that uses high-throughput sequencing, we report the first genome-wide distribution of 8-oxodG in human cells, using the non-tumorigenic epithelial breast cells MFC10A. Results were compared with those we obtained in mouse embryo fibroblasts. OxyDIP-Seq revealed sites of 8-oxodG accumulation overlapping with gH2AX ChIP-Seq signals within gene bodies of long transcribed genes.

2018-11-28 | GSE100234 | GEO

Genome-wide analysis gene expression of MCF10A cells growing in the presence of EGF or AREG or without EGF or AREG for 24 hrs

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Genome-wide analysis gene expression of MCF10A cells growing in the presence of EGF or AREG or without EGF or AREG for 24 hrs

Project description:Results of growing MCF10A cells continuously in serum free media supplemented with EGF (MCF10A) or AREG (MCF10A+AREG) followed by 24 hours of ligand withdrawl and measuring gene expression provides information as to what genes are regulated by AREG and EGF in a normal mammary epithelial cell model MCF10A cells continuously in serum free media supplemented with 10ng/ml of EGF (MCF10A) or 20ng/ml of AREG (MCF10A+AREG) followed by 24 hours of ligand withdrawl. Total RNA was collected and genome-wide analysis of expression was performed on RNA from each cell line.

2010-12-23 | E-GEOD-26264 | biostudies-arrayexpress

Genome-wide mapping of 8-oxodG in G0-arrested MCF10A cells

Project description:Genome-wide mapping of 8-oxodG in G0-arrested MCF10A cells

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Genome-wide mapping of 8-oxodG in G0-arrested MCF10A cells

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Genome wide mapping of gH2AX in quiescent and irradiation-induced senescent human fibroblasts

Project description:We observe preferential accumulation of gH2AX at chromosome ends upon irradiation comparison of quiescent vs senescent human fibroblasts

2012-03-13 | E-GEOD-35884 | biostudies-arrayexpress

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Project description:We observe preferential accumulation of gH2AX at chromosome ends upon irradiation

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Expression Data from wild type and E2F4 null MEFs

Project description:We have used primary MEFs derived from wild type and E2F4 null mice growing asynchrounously in serum to generate a signature for E2F4 pathway activation. 10 wild type and 10 E2F4 null samples were each assayed using the Affymetrics Mouse Genome 430A 2.0 array. Keywords: Primary MEFs from wild type and E2F4 null mice

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Genomic binding of RUNX1 in MCF10A cells

Project description:The overall goal of this study is to identify the genomic binding of RUNX1 in MCF10A cells. We used ChIPseq (chromatin immunoprecipitation assay followed by deep sequencing) to identify the binding sites of RUNX1 in MCF10A cells. We performed ChIPseq of RUNX1 using parental MCF10A cells and did not identify high confident binding sites. To overcome this hurdle, we first generated a RUNX1 deleted MCF10A cell line using CRISPR-Cas9. We then transduced this RUNX1 KO MCF10A cells with lentiviruses that inducibly expresses RUNX1. After treating RUNX1 inducible MCF10A cells with 1 ug/ml doxycycline for 24 hours, we performed ChIPseq of RUNX1.

2019-04-18 | GSE129314 | GEO

Genome-wide analysis of H3.3, H3K36me2, H3K36me3 and ZMYND11 accumulation in WT MEFs and NSD2 KO MEFs.

Project description:We found that the incorporation of histone H3 variant H3.3 was impaired and the accumulation of ZMYND11, which specifically binds to H3.3K36me3, was decreased in NSD2 KO MEFs. About H3K36me2, the average gene body profiles of H3K36me2 showed preferential enrichment of H3K36me2 at the promoter and first half of the genic regions. We examined H3K36me2 mark in super enhancer regions using the ROSE super enhancer prediction program and identified of the 519 super enhancer islands of H3K36me2 in WT MEFs the H3K36me2 signals were decreased in NSD2 KO MEFs

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