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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genomic landscape of Epstein-Barr virus nuclear antigen 3A

ABSTRACT: We undertook ChIP-Seq of HA-tagged EBNA3A in Lymphoblastoid Cell Lines to understand the effects of this essential viral transcription factor on the cell DNA. We discovered that EBNA3A bound to DNA with BATF, IRF4 and RUNX3, making these Transcription Factors the ones that tether EBNA3A to DNA, allowing it to mediate its downstream effects. ChIP-Seq of 2 biological replicates of HA-tagged EBNA3A were performed. Input was obtained by reverse-crosslinking the cross-linked DNA

ORGANISM(S): Homo sapiens

SUBMITTER: Hufeng Zhou

PROVIDER: E-GEOD-59181 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Epstein-Barr virus nuclear antigen 3A partially coincides with EBNA3C genome-wide and is tethered to DNA through BATF complexes.

Schmidt Stefanie C S SC Jiang Sizun S Zhou Hufeng H Willox Bradford B Holthaus Amy M AM Kharchenko Peter V PV Johannsen Eric C EC Kieff Elliott E Zhao Bo B

Proceedings of the National Academy of Sciences of the United States of America 20141224 2

Epstein-Barr Virus (EBV) conversion of B-lymphocytes to Lymphoblastoid Cell Lines (LCLs) requires four EBV nuclear antigen (EBNA) oncoproteins: EBNA2, EBNALP, EBNA3A, and EBNA3C. EBNA2 and EBNALP associate with EBV and cell enhancers, up-regulate the EBNA promoter, MYC, and EBV Latent infection Membrane Proteins (LMPs), which up-regulate BCL2 to protect EBV-infected B-cells from MYC proliferation-induced cell death. LCL proliferation induces p16(INK4A) and p14(ARF)-mediated cell senescence. EBNA ...[more]

PMID: 25540416

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Genomic landscape of Epstein-Barr virus nuclear antigen 3A

Project description:We undertook ChIP-Seq of HA-tagged EBNA3A in Lymphoblastoid Cell Lines to understand the effects of this essential viral transcription factor on the cell DNA. We discovered that EBNA3A bound to DNA with BATF, IRF4 and RUNX3, making these Transcription Factors the ones that tether EBNA3A to DNA, allowing it to mediate its downstream effects.

2015-01-06 | GSE59181 | GEO

EBNA3 proteins regulate EBNA2 binding to distinct RBPJ genomic sites

Project description:We report the application of ChIP Seq to study the Epstein Barr Virus Nuclear Antigen EBNA3A, EBNA3B, EBNA3C, an essential transcriptional regulator involved in the transformation of Resting B Lymphocytes to the immortalized Lymphoblast Cell Lines. Examination of EBNA3A, EBNA3B and EBNA3C protein genome binding in LCLs.

2016-01-05 | E-GEOD-76166 | biostudies-arrayexpress

The NF-kB genomic landscape in lymphoblastoid B-cells

Project description:The nuclear factor kB (NF-kB) subunits RelA, RelB, c-Rel, p50 and p52 are each critical for B-cell development and function. To systematically characterize their responses to canonical and non-canonical NF-kB pathways activity, we performed ChIP-seq analysis in lymphoblastoid B-cells. We found a surprisingly complex NF-kB binding landscape, which did not readily reflect the two NF-kB pathway paradigm. Instead, ten subunit binding patterns were observed at promoters and eleven at enhancers. Surprisingly, nearly one-third of NF-kB binding sites lacked kB motifs. De novo motif finding uncovered distinct modes of NF-kB recruitment at these sites. The oncogenic forkhead box protein FOXM1 and NF-kB co-occupied many kB sites despite the absence of a FOXM1 DNA motif. FoxM1 knockdown decreased expression of key NF-kB targets and caused apoptosis. Our study highlights opportunities for selective therapeutic NF-kB blockade. ChIP-seq was used to define the genomic landscape of NF-kB DNA binding in lymphoblastoid cells.

2014-08-29 | E-GEOD-55105 | biostudies-arrayexpress

Epstein Barr Virus Nuclear Antigen 3C binds to BATF/IRF4/SPI1 sites and represses CDKN2A by recruiting Sin3A

Project description:We report the application of ChIP Seq to study the Epstein Barr Virus Nuclear Antigen 3C, an essential transcriptional regulator involved in the transformation of Resting B Lymphocytes to the immortalized Lymphoblast Cell Lines Examination of viral and cellular transcription factors in 1 type of cell line

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Epstein-Barr Virus oncoprotein super-enhancers control B cell growth

Project description:Super-enhancers are principal determinants of cell transcription, development, phenotype, and oncogenesis, not yet implicated in host-pathogen interactions. We found four Epstein-Barr virus (EBV) oncoproteins and five EBV-activated NF-M-oM-^AM-+B subunits co-occupying thousand of enhancer sites in EBV-transformed lymphoblastoid cells (LCLs). Of these, 187 had markedly higher and broader histone H3K27ac signals characteristic of super-enhancer formation, and were designated M-bM-^@M-^\EBV super-enhancersM-bM-^@M-^]. EBV super-enhancer associated genes included MYC and BCL2, which enable LCL proliferation and survival. EBV super-enhancers were enriched for specific B cell transcription factor motifs and had high STAT5 and NFAT co-occupancy. EBV super-enhancer associated genes were more highly expressed than other LCL genes. Disruption of EBV super-enhancers by the bromo-domain inhibitor, JQ1, by conditional inactivation of an EBV oncoprotein or NF-M-oM-^AM-+B, decreased MYC or BCL2 gene expression and arrested LCL growth. These findings provide novel insights into the mechanisms by which EBV causes lymphoproliferation and identify opportunities for therapeutic intervention. ChIP-seq was used to define the BRD4 genome-wide landscape in GM12878 lymphoblastoid cells.

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2014-07-24 | E-GEOD-57900 | biostudies-arrayexpress

ChIP-exo analysis of the DNA-binding sites of the yeast transcription factor Yfl052w sequenced by SOLiD

2014-07-24 | E-GEOD-57901 | biostudies-arrayexpress

Convergence of distinct RNA-silencing pathways on GW182/Tnrc6 [RIP-seq]

Project description:RIP-sequencing in mouse embryonic stem cells. Experiment 1 (Samples 1-18): Base cell line (untagged control cells): GFP_5xT71BS (mES [129S6/SvEvTac], yGlob [GFP_5xT71BS], stable transfection FLAG-Cas9::T2A::Blasticidin). HA-Tnrc6a: endogenously HA-AVI-tagged Tnrc6a. HA-Tnrc6a_Trim71KO: HA-AVI-tagged Tnrc6a, Trim71-/-. Experiment 2 (Samples 19-42): Ctrl: base cell line GFP_5xT71BS. Tnrc6a: endogenously HA-AVI-tagged Tnrc6a. Tnrc6a_Trim71KO: HA-AVI-tagged Tnrc6a, Trim71-/-. Tnrc6a_Ago2KO: HA-AVI-tagged Tnrc6a, Ago2-/-.

2023-06-26 | GSE205966 | GEO

Convergence of distinct RNA-silencing pathways on GW182/Tnrc6 [RIP-seq II]

Project description:RIP-sequencing in mouse embryonic stem cells. Experiment 3 (Samples 2-24) & 4 (Samples 25-48): Base cell line (untagged control cells): GFP_5xT71BS (mES [129S6/SvEvTac], yGlob [GFP_5xT71BS], stable transfection FLAG-Cas9::T2A::Blasticidin). HA-Tnrc6a: endogenously HA-AVI-tagged Tnrc6a. HA-Tnrc6a_Trim71KO: HA-AVI-tagged Tnrc6a, Trim71-/-. Experiment 2 (Samples 19-42): Ctrl: base cell line GFP_5xT71BS. Tnrc6a: endogenously HA-AVI-tagged Tnrc6a. Tnrc6a_Trim71KO: HA-AVI-tagged Tnrc6a, Trim71-/-. Tnrc6a_Ago2KO: HA-AVI-tagged Tnrc6a, Ago2-/-.

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