Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

41 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

ABSTRACT: We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of H3K4me3 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle

ORGANISM(S): Homo sapiens

SUBMITTER: Xuting Wang

PROVIDER: E-GEOD-51713 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle

2013-10-23 | E-GEOD-46991 | biostudies-arrayexpress

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with nutlin-3

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a MDM2 inhibitor nutlin-3 ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with nutlin-3 or vehicle

2013-10-23 | E-GEOD-46992 | biostudies-arrayexpress

Identification of Novel NRF2-Regulated Genes by ChIPSeq

Project description:Cellular oxidative and electrophilic stress triggers a protective response in mammals regulated by NRF2 (nuclear factor (erythroid-derived) 2-like; NFE2L2) binding to DNA-regulatory sequences near stress responsive genes. Studies using Nrf2-deficient mice suggest that hundreds of genes may be regulated by NRF2. To identify human NRF2-regulated genes, we conducted ChIP-sequencing experiments in lymphoid cells treated with the dietary isothiocyanate, sulforaphane (SFN) and carried out follow-up biological experiments on candidates. We found 242 high-confidence, NRF2-bound genomic regions and 96% of these regions contained NRF2-regulatory sequence motifs. The majority of binding sites were near potential novel members of the NRF2 pathway. Validation of selected candidate genes using parallel ChIP techniques and in NRF2-silenced cell lines indicated that the expression of about two thirds of the candidates are likely to be directly NRF2-dependent including retinoid X receptor alpha (RXRA). NRF2 regulation of RXRAhas implications for response to retinoid treatments and adipogenesis. In mouse 3T3-L1 cells SFN treatment affected Rxra expression early in adipogenesis and knockdown of Nrf2 delayed Rxra expression, both leading to impaired adipogenesis. ChIP-Seq analysis of NRF2 binding sites in human lymphoblastoid cells treated with sulforaphane or vehicle

2012-06-18 | E-GEOD-37589 | biostudies-arrayexpress

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with ionizing radiation

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated withionizing radiation ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with ionizing radiation or vehicle

2013-10-23 | E-GEOD-46993 | biostudies-arrayexpress

Gene expression in human lymphoblastoid cell-line GM12878 in response to doxorubicin treatment

Project description:To determine if induced p53 binding is associated with gene expression in genome-wide. We examined mRNA levels with the Affymetrix Human Exon 1.0 ST platform in human lymphoblastoid GM12878 cells treated with doxorubicin to activate p53. In response to various cellular stresses, the tumor suppressor gene p53 induces activation or repression of more than a thousand human genes. Selective binding and transactivation of a large potential pool of p53 response elements (REs) is believed to regulate the variation in stress response across stress types and between cell types. To elucidate how the human genome is targeted by p53 at the chromatin level, we mapped the genome-wide localization of p53 and H3K4me3 from Doxo-treated human lymphoblastoid cells, and examined the relationships among p53 occupancy, gene expression, H3K4me3, chromatin accessibility (DNase 1 Hypersensitivity, DHS), ENCODE chromatin states, RE sequence specificity and evolutionary conservation. Human lymphoblastoid (GM 12878) cells at a density of 900,000 cells/ml were prepared in triplicate for each time point and treated with 0.5 µM doxorubicin (Calbiochem) for 4, 18 hr or no treatment (at 0 time). Total RNA will be extracted from each culture (9 RNA samples) using the Qiagen RNeasy kit with DNase digestion. RNA was quantified using RiboGreen (Invitrogen), check for quality by OD and Bioanalyzer and stored at -80°C. Expression analysis was conducted at at NIEHS Microarray Core using Affymetrix Human Exon 1.0 ST arrays following the Affymetrix hybridization protocols. Exon expression data were analyzed through Affymetrix Expression Console using gene-level RMA summarization and sketch-quantile normalization methods.

2014-11-14 | E-GEOD-51709 | biostudies-arrayexpress

p53 activation effect on GM12878 lymphoblastoid cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-11-14 | E-GEOD-51714 | biostudies-arrayexpress

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader ProteinM-BM- (EBNALP)

Project description:Epstein-Barr-Virus (EBV) Nuclear Antigens EBNALP and EBNA2 are co-expressed in EBV infected B-lymphocytes and are critical for Lymphoblastoid Cell Line (LCL) growth. EBNALP removes NCOR1 and RBPJ repressive complexes from promoter and enhancer sites and EBNA2 mostly activates transcription from distal enhancers. ChIP-seqs found EBNALP at 19,224 LCL sites, which were 33% promoter associated. EBNALP was associated with 10 transcription factor (TF) clusters that included YY1(63%), SP1(62%), PAX5(59%), BATF(50%), IRF4(49%), RBPJ(43%), ETS1(39%), PU.1(37%), RAD21(33%), NF-kB(31%), TBLR1(26%), ZNF143(24%), CTCF(23%), SMC3(21%), and EBF(17%). EBNALP sites had higher H3K4me3, H3K9ac, H3K27ac, H2Az, and RNA Pol II signals than EBNA2 sites and had similar transcription effects. EBNALP co-localized with 29% of 19,845 EBNA2 sites. EBNALP/EBNA2 sites were similar to EBNALP sites in promoter localization, associated cell TFs, Pol II, H3K4me3, H3K9ac, H3K27ac, and H2Az signals. EBNALP and EBNA2 promoter sites were more transcriptionally active than EBNALP or EBNA2 promoter sites. EBNALP was at the enhancer or promoter of myc and MYC affected genes, including cyclin D2, and bcl2. EBNALP at promoters with DNA looping and transcription factors, is positioned to deplete repressors from enhancers and promoters, enable chromatin remodeling, and transcription activation. Two EBNALP ChIP-seq replicates from IB4 LCL are analyzed in this study.

2013-07-31 | E-GEOD-49338 | biostudies-arrayexpress

Genome-wide target discovery of transcripton factor E2F4 by ChIP-seq

Project description:The transcription factor E2F4 is a member of the E2F family of regulators which has critical roles in cell cycle control and differentiation. In order to fully understand the physiological roles of E2F4 and the regulatory networks it mediates, and to reveal its relationships with other members of the E2F family, it is essential to comprehensively identify E2F4 target sites throughout the genome. Here, we investigated genome-wide E2F4 targets in human lymphoblastoid cells using the recently developed unbiased target discovery technique of ChIP sequencing. We sequecned E2F4 ChIP and corresponding Input

2010-11-01 | E-GEOD-21488 | biostudies-arrayexpress

Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin.

2014-11-14 | GSE51713 | GEO

Epigenetic changes due to histone eviction induced by anthracycline doxorubicin and aclarubicin

Project description:One major class of anti-cancer drugs targets topoisomerase II to induce DNA double-strand breaks and cell death of fast growing cells. Here, we compare three members of this class - the antracyclines doxorubicin and aclarubicin, and a chemically unrelated compound, etoposide. Aclarubicin does not induce DNA breaks. We define a new activity for the antracyclines: unsupported histone eviction from ´open´ or loosely packed chromosomal areas reflecting exon and promoter regions. Comparison of histone H3K4me3 of cells post topoisomerase II inhibitors treatment to un-treated ones by ChIP-seq. Comparison of phosphorylated histone H2AX of cells post topoisomerase II inhibitors doxorubicin and etoposide treatment to un-treated ones by ChIP-seq.

2013-06-04 | E-GEOD-33633 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data