Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

19 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Hufeng Zhou

PROVIDER: E-GEOD-49338 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

ChIP-seq data of Epstein-Barr Virus Nuclear Antigen Leader Protein (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.

2013-07-31 | GSE49338 | GEO

Epstein-Barr Virus Exploits Intrinsic B-Lymphocyte Transcription Programs to Achieve Immortal Cell Growth

Project description:Epstein-Barr Virus Nuclear Antigen 2 (EBNA2) gene regulation through the cell RBPJ transcription factor (TF) is essential for conversion of resting B-lymphocytes (RBLs) into Lymphoblastoid Cell Lines (LCLs). ChIP-seq investigation of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5151 and RBPJ at 10,529 sites. EBNA2 was 72% localized with RBPJ, predominantly at intergenic and intronic sites and only 14% at promoter sites. EBNA2/RBPJ sites were enriched for Early B-cell Factor (EBF, 60%), RUNX(41%), ETS(35%), NF-ï«B(31%), and PU.1(17%) TF motifs. Using ENCyclopedia Of DNA Elements (ENCODE) LCL data, EBF, RELA, and PU.1 were found at 54%, 31%, and 17% of EBNA2 sites. K-Means clustering of EBNA2 site associated TFs found RELA-ETS, EBF-RUNX, EBF, ETS, RBPJ, and repressive RUNX ranked highest to lowest in nearly symmetric H3K4me1 signal distribution and nucleosome depletion, marks of active chromatin. Although quantitatively less, high level nearly symmetric H3K4me1 signals with nucleosome depletion at the same sites in RBLs was remarkably similar to LCLs, indicating that EBNA2 localizes into a pre-established RBL chromatin pattern, which likely evolved to enable RBL antigen-induced proliferation. EBF was critical for EBNA2 activation of the EBV LMP1 promoter. LCL HiC data mapped intergenic EBNA2 sites to EBNA2 up-regulated genes. Fluorescence In Situ Hybridization (FISH), conditional EBNA2 FISH, Chromatin Conformation Capture (3C), and 3C q-PCR, linked EBNA2/RBPJ enhancers 428 kb 5' of MYC to MYC. These data support the hypothesis that EBNA2 evolved to exploit the RBL transcription framework to drive B-lymphocyte proliferation in primary human infection. EBNA2 and RBPJ ChIP-seq from IB4 LCL

2011-07-01 | E-GEOD-29498 | biostudies-arrayexpress

Epstein-Barr Virus Exploits Intrinsic B-Lymphocyte Transcription Programs to Achieve Immortal Cell Growth

2011-07-01 | GSE29498 | GEO

Chromatin immunopreciptation genome wide location of H2A.Z binding sites in yeast yeast

Project description:genome wide location of H2A.Z binding sites in yeast Saccharomyces cerevisiae. Nucleosome density controled with H2B ChIP. Hybridization control ChIP H2AZ/H2AZ and H2A/H2B.

2005-12-31 | E-MEXP-396 | biostudies-arrayexpress

MYC activation and BCL2L11 silencing by a tumor virus through the large-scale reconfiguration of enhancer-promoter hubs [EREB]

Project description:Lymphomagenesis in the presence of deregulated MYC expression requires suppression of MYC-driven apoptosis, often through downregulation of the pro-apoptotic BCL2L11 gene (Bim). Transcription factors (EBNAs) encoded by the lymphoma-associated Epstein-Barr virus (EBV) activate MYC and silence BCL2L11. We show that EBNA2 upregulates MYC by reconfiguring the 3 Mb MYC locus to increase upstream and decrease downstream enhancer-promoter interactions. EBNA2 recruits the SWI/SNF ATPase BRG1 to drive MYC enhancer-promoter interactions. MYC-Immunoglobulin translocation breakpoints in EBV-positive endemic Burkitt lymphoma localise to EBNA2-activated upstream MYC regions. This implicates EBV in the genesis and localisation of breakpoints, since active enhancers are targeted by activation-induced cytidine deaminase. We identify a novel haematopoietic BCL2L11 enhancer hub that is inactivated by EBNA3A and EBNA3C through recruitment of the H3K27 methyltransferase EZH2. Reversal of enhancer inactivation using an EZH2 inhibitor upregulates BCL2L11 and induces apoptosis. EBV therefore drives lymphomagenesis by hijacking long-range enhancer hubs and specific cellular co-factors. A study of MYC enhancer-promoter interactions using 4C on induction of MYC by the Epstein-Barr virus transcription factor EBNA2 in a lymphoblastoid cell line.

2016-08-04 | E-GEOD-82149 | biostudies-arrayexpress

Combinatorial Control of RBP-jk and EBF1 Chromosome Occupancy induced by viral co-activator EBNA2 [ChIP-seq]

Project description:Gene expression programs depend on sequence-specific DNA binding transcription factors, but the mechanisms that control the selective binding of these factors in a chromosomal and genomic context remain enigmatic. Here, we show that two master regulators of B-cell fate, namely EBF1 and RBP-jk, show variable genome-wide chromosome distribution in two related B-lymphocyte lines carrying different forms of Epstein-Barr Virus (EBV) latency. The latency-type specific EBV-encoded EBNA2 colocalized with RBP-jk and EBF1 at induced binding sites. Colocalization of EBF1, RBP-jk, and EBNA2 correlated with transcriptional activation. Conditional expression or repression of EBNA2 lead to a rapid alteration in RBP-jk and EBF1 binding. Biochemical and shRNA depletion studies provide evidence for cooperative assembly at co-occupied sites. These findings reveal that non-DNA binding cofactors can facilitate combinatorial interactions to induce new patterns of transcription factor occupancy and gene programming Examination of EBNA2/EBF1/EBP-jk binding in MutuI and LCL cell lines

2015-12-16 | E-GEOD-75503 | biostudies-arrayexpress

Genome-wide Analysis Reveals Conserved and Divergent Features of Notch1/RBPJ Binding in Human and Murine T Lymphoblastic Leukemia Cells

Project description:Notch1 regulates gene expression by associating with the DNA-binding factor RBPJ and is oncogenic in murine and human T cell progenitors. Using ChIP-Seq, we find that in human and murine T-LL genomes Notch1 binds preferentially to promoters, to RBPJ binding sites, and near imputed ZNF143, Ets and Runx sites. ChIP-Seq confirmed that ZNF143 binds to ~40% of Notch1 sites. Notch1/ZNF143 sites are characterized by high Notch1 and ZNF143 signals, frequent co-binding of RBPJ (generally through sites embedded within ZNF143 motifs), strong promoter bias, and relatively low mean levels of activating chromatin marks. RBPJ and ZNF143 binding to DNA is mutually exclusive in vitro, suggesting RBPJ/Notch1 and ZNF143 complexes exchange on these sites in cells. K-means clustering of Notch1 binding sites and associated motifs identified conserved Notch1-Runx, Notch1-Ets, Notch1-RBPJ, Notch1-ZNF143, and Notch1-ZNF143-Ets clusters with different genomic distributions and levels of chromatin marks. Although Notch1 binds mainly to gene promoters, ~75% of direct target genes lack promoter binding and are presumably regulated by enhancers, which were identified near MYC, DTX1, IGF1R, IL7R and the GIMAP cluster. Human and murine T-LL genomes also have many sites that bind only RBPJ. Murine RBPJ M-CM-"M-BM-^@M-BM-^\onlyM-CM-"M-BM-^@M-BM-^] sites are highly enriched for imputed REST sites, whereas human RPBJ M-CM-"M-BM-^@M-BM-^\onlyM-CM-"M-BM-^@M-BM-^] sites lack REST motifs and are more highly enriched for imputed CREB sites. Thus, there is a conserved network of cis-regulatory factors that interacts with Notch1 to regulate gene expression in T-LL cells, as well as novel classes of divergent RBPJ M-CM-"M-BM-^@M-BM-^\onlyM-CM-"M-BM-^@M-BM-^] sites that also likely regulate transcription. Notch1, RBPJ, histone methylation ChIP-seq in human and mouse T-LL cell lines

2011-07-06 | E-GEOD-29600 | biostudies-arrayexpress

MYC activation and BCL2L11 silencing by a tumor virus through the large-scale reconfiguration of enhancer-promoter hubs [Bcell]

Project description:Lymphomagenesis in the presence of deregulated MYC expression requires suppression of MYC-driven apoptosis, often through downregulation of the pro-apoptotic BCL2L11 gene (Bim). Transcription factors (EBNAs) encoded by the lymphoma-associated Epstein-Barr virus (EBV) activate MYC and silence BCL2L11. We show that EBNA2 upregulates MYC by reconfiguring the 3 Mb MYC locus to increase upstream and decrease downstream enhancer-promoter interactions. EBNA2 recruits the SWI/SNF ATPase BRG1 to drive MYC enhancer-promoter interactions. MYC-Immunoglobulin translocation breakpoints in EBV-positive endemic Burkitt lymphoma localise to EBNA2-activated upstream MYC regions. This implicates EBV in the genesis and localisation of breakpoints, since active enhancers are targeted by activation-induced cytidine deaminase. We identify a novel haematopoietic BCL2L11 enhancer hub that is inactivated by EBNA3A and EBNA3C through recruitment of the H3K27 methyltransferase EZH2. Reversal of enhancer inactivation using an EZH2 inhibitor upregulates BCL2L11 and induces apoptosis. EBV therefore drives lymphomagenesis by hijacking long-range enhancer hubs and specific cellular co-factors. A study of MYC enhancer-promoter interactions using 4C on induction of MYC by Epstein-Barr virus infection of CD19+ primary B cells. B cells physiologically activated by treatment with CD40 ligand and IL-4 were studied as a control.

2016-08-04 | E-GEOD-82148 | biostudies-arrayexpress

Homo sapiens

Project description:EBNA3 proteins regulate EBNA2 binding to distinct RBPJ genomic sites

| PRJNA306509 | ENA

Comparative ChIP-chip analysis of general transcription factor TFIIB and negative cofactor NC2 in human B cells

Project description:A comparative ChIP-chip analysis of TFIIB and NC2 in human B cells reveals that basal core promoter architectures control the equilibrium between NC2 and preinitiation complexes. We conducted a comparative ChIP-chip and gene expression analysis of TFIIB in human B cells and analyze associated core promoter architectures. TFIIB occupancy relates well to gene expression, with the vast majority of promoters being GC-rich and lacking defined core promoter elements. TATA consensus and TATA-like motifs but not the previously in vitro defined TFIIB recognition elements (BREs) are enriched in approximately 5% of the genes. Further insight was obtained by performing a parallel ChIP-chip analysis of the TFIIB antagonist NC2. The latter identifies a highly related target gene set. Nonetheless, subpopulations show strong variations in TFIIB/NC2 ratios, with high NC2/TFIIB ratios correlating to promoters that show dispersed transcription start site patterns and lacking defined core elements. Conversely, high TFIIB/NC2 ratios select for conserved core promoter elements that include TATA and INR (initiator), the upstream TFIIB recognition element (BREu) and the downstream promoter element (DPE). Two biological samples from LCL 721 lymphoblastoid human B cells were subjected to ChIP-chip analysis of TFIIB and NC2 using a Nimblegen human promoter array (based on the HG17 genome build) covering 1.5 kb DNA around transcription start sites.

2010-05-16 | E-GEOD-19562 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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