Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA306509 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3033170.fastq.gz | Fastqsanger.gz | |||
| SRR3033171.fastq.gz | Fastqsanger.gz | |||
| SRR3033172.fastq.gz | Fastqsanger.gz |
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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
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.
2011-07-01 | GSE29498 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246061 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246060 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246059 | GEO
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
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
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
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 âonlyâ sites are highly enriched for imputed REST sites, whereas human RPBJ âonlyâ 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 âonlyâ sites that also likely regulate transcription.
2011-07-06 | GSE29600 | GEO
Project description:From the cell-based investigation, RBPJ is one of the few proteins retained on chromatin during cell division. ChIP-seq experiments were performed to understand the binding pattern of RBPJ between interphase and mitosis and to identify the genes requiring RBPJ binding for the maintenance of transcriptional memory. Our results indicate that ~60% of RBPJ occupancy in interphase is retained on mitotic chromatin, and that accounts for 80% of RBPJ in mitosis. The gene ontology analysis reveals that the genes involved in stem cell maintenance, development and differentiation-related pathways correlated with sites of RBPJ occupancy. GO analysis also suggests that RBPJ plays a role in the metabolism and processing of non-coding RNAs. Motif analysis of RBPJ binding sites reveals that not only RBPJ motif but also CTCF motif are enriched around RBPJ binding sites. From these results, we propose that RBPJ can function as a mitotic bookmark, marking genes for efficient transcriptional activation or repression upon exit from mitosis, and may play a role in higher order chromatin structure by collaborating with CTCF. To compare the genomic RBPJ localization in mitotic and interphase cells, mouse F9 cells were harvested and labeled as cycling cells (containing 95% interphase and 5% mitosis cells); nocodazole treated F9 cells were harvested and labeled as mitotic cells. Cell samples were proceeded to ChIP-seq experiments, and each of the experiment contains a set of ChIP DNA product: input as the background control and IP as the RBPJ binding product. Background noise was substracted and the obtained signal was used for the comparison of interphase and mitosis by statistical analysis. Please note that processed data (*bed) was generated from *rep1 sample (i.e. no processed-data for rep2 sample).
2014-05-14 | E-GEOD-45889 | biostudies-arrayexpress