Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1309881 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To test the effects of uracil DNA glycosylase (UNG) loss on the formation of double strand breaks (DSBs) by the anti-cancer agent pemetrexed, we performed ChIP-seq for serine 139-phosphorylated H2AX (gammaH2AX), a marker of DSBs, in human cells wild-type or deficient for UNG in combination with pemetrexed treatment. UNG deficiency results in an increase in DSBs upon pemetrexed treatment, and we found that pemetrexed treatment induces DSBs at different genomic locations in UNG wild-type and knockout cells. Similar results were observed upon cisplatin treatment of UNG wild-type and knockout cells, and the genomic locations of DSBs were distinct between pemetrexed-treated and cisplatin-treated samples. Taken together, our results suggst differential mechanisms for DSB formation in UNG-competent and UNG-deficient cells. The genomic distribution of gammaH2AX in UNG WT and KO cells treated with pemetrexed or cisplatin was determined by ChIP-seq
2013-10-28 | E-GEOD-50692 | biostudies-arrayexpress
Project description:Gene expression and pre-mRNA splicing events were examined in human breast adenocarcinoma (MCF7) cells treated or not with cisplatin and various siRNAs.
2022-11-05 | GSE195842 | GEO
Project description:MCF7 cells untreated and treated with cisplatin at 50µM for 24 hours.
2016-04-22 | E-MTAB-2663 | biostudies-arrayexpress
Project description:Genome-wide distribution of histone H3K18 and H3K27 acetyltransferases, Crebbp (CBP) and Ep300 (p300), is used to map enhancers and promoters, but whether these elements functionally require CBP/p300 remains largely uncertain. We investigated this relationship by comparing genomic CBP recruitment with gene expression in wild type and CBP/p300 double-knockout fibroblasts. ChIP-seq revealed nearby CBP recruitment for 20 percent of constitutively expressed genes, but surprisingly, three-quarters of these were unaffected or slightly activated by CBP/p300 deletion. Computationally defined enhancer-promoter-units (EPUs) having a CBP peak within two kilobases of the enhancer-like element provided better predictive value, with CBP/p300 deletion attenuating expression of 40 percent of such EPU assigned constitutively expressed genes. We next examined signaling-responsive (Hypoxia Inducible Factor) gene expression and CBP recruitment, and found that 97 percent of inducible genes were within 50 kilobases of an inducible CBP peak, and 70 percent of these required CBP/p300 for full inducible expression. Unexpectedly however, most inducible CBP peaks occurred near signal-nonresponsive genes. eight samples total; Two wild type and two CBP null primary mouse embryonic fibroblast (MEF) lines, each treated with 100uM 2,2-dipyridyl or ethanol vehicle for 2 hours
2014-09-29 | E-GEOD-54453 | biostudies-arrayexpress
Project description:We report the genome wide occupancy of p65, H3K4Me3, H3K27Ac and p300 in MCF7-NAIL-WT and MCF7-NAIL-ΔNFκB cells stimulated with TNF alpha for 0min, 45min and 90 min.
2023-09-01 | GSE138308 | GEO
Project description:Treatment of MCF7 breast cancer cells by cisplatin leads to a very specific metabolic response and an onset of cell death about 10-11 h after beginning of treatment. For more detailed understanding of the molecular processes underlying the specific metabolic response, mRNA was isolated from MCF7 cells when the specific changes, (i) induction of glycolysis and (ii) onset of cell death, were detected during online measurement in the cell biosensor system. MCF7 breast cancer cells were treated with cisplatin in the BIONAS 2500 cell biosensor chip system, and samples were collected from the biosensor chip module at time points when glycolysis was induced (change of ph; 8-9h) and at the beginning of cell death (change of impedance; 10-11h).
2011-04-04 | E-GEOD-28274 | biostudies-arrayexpress
Project description:We characterize the acetylation of H3K122 for the first time. Towards this we mapped the genomic distribution of H3K122Ac, identified the enzyme introducing H3K122Ac, and addressed the functional contribution H3K122Ac to transcription. We found that H3K122Ac is associated with chromatin marks and genomic regions associated with active transcription and is catalysed by p300/CBP and can be regulated by estrogen signaling in MCF-7. Moreover H3K122Ac stimulates transcription as dermined by in vitro transcription assays ChIP seq study
2013-02-14 | E-GEOD-35954 | biostudies-arrayexpress
Project description:Genome-wide distribution of histone H3K18 and H3K27 acetyltransferases, Crebbp (CBP) and Ep300 (p300), is used to map enhancers and promoters, but whether these elements functionally require CBP/p300 remains largely uncertain. We investigated this relationship by comparing genomic CBP recruitment with gene expression in wild type and CBP/p300 double-knockout fibroblasts. ChIP-seq revealed nearby CBP recruitment for 20 percent of constitutively expressed genes, but surprisingly, three-quarters of these were unaffected or slightly activated by CBP/p300 deletion. Computationally defined enhancer-promoter-units (EPUs) having a CBP peak within two kilobases of the enhancer-like element provided better predictive value, with CBP/p300 deletion attenuating expression of 40 percent of such EPU assigned constitutively expressed genes. We next examined signaling-responsive (Hypoxia Inducible Factor) gene expression and CBP recruitment, and found that 97 percent of inducible genes were within 50 kilobases of an inducible CBP peak, and 70 percent of these required CBP/p300 for full inducible expression. Unexpectedly however, most inducible CBP peaks occurred near signal-nonresponsive genes. 12 samples, 3 each wild type and CBP/p300 null treated for 3hrs with 100uM dipyridyl orethanol vehicle.
2014-09-29 | E-GEOD-54452 | biostudies-arrayexpress
Project description:Human primary hepatic stellate cells were purchased from ScienCell Research Laboratories. To identify TGFβ transcription targets and those are also modulated by p300 acetyltransferase, cells were treated with C646 to inhibit p300 acetyltransferase or transduced with p300 shRNA to knockdown p300. Thus, cell were divided into 4 groups: cells treated with DMSO, cells treated with C646 (15 uM), cells transduced with control shRNA, and cells transduced with p300 shRNA. After cells were serum-starved, they were stimulated with or without TGF-beta for 24 hours. Total RNA was then extracted and sent to University of Minnesota Genomic Center for microarray analysis.
2018-07-03 | GSE116509 | GEO