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Transcriptome analysis of CHAF1B depletion in Akata EBV+ Burkitt Lymphoma cells

ABSTRACT: Transcriptome analysis of CHAF1B depletion in Akata EBV+ Burkitt Lymphoma cells

PROVIDER: PRJNA626463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11570100_1.fastq.gz	Fastqsanger.gz
	SRR11570100_2.fastq.gz	Fastqsanger.gz
	SRR11570101_1.fastq.gz	Fastqsanger.gz
	SRR11570101_2.fastq.gz	Fastqsanger.gz
	SRR11570102_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of CHAF1B depletion in Akata EBV+ Burkitt Lymphoma cells

Project description:RNAseq was used to identify host and EBV viral transcriptome changes in CHAF1B knock-out Akata EBV+ cells. CHAF1B KO Akata EBV+ cells were subjected to RNAseq analysis. The Akata EBV+ cells expressing control sgRNA was used as the control.

2020-10-15 | GSE148910 | GEO

Transcriptomic analysis of LMP1 TES domain single or double mutant in EBV-negative Akata Burkitt Lymphoma Cells

Project description:RNA-seq was used to characterize the LMP1 TES domain-mediated regulation of B-cell genome wide target genes. We created an inducible stable EBV-negative Akata Burkitt Lymphoma cell line expressing LMP1 wildtype, TES1 functional only, TES2 functional only and TES1/2 non-functional.

2023-04-25 | GSE228178 | GEO

Transcriptomic analysis of EBV-negative Akata Burkitt Lymphoma Cell target genes upon CRISPR knockout of the individual NF-κB transcription factor as well as induction of wildtype LMP1 expression

Project description:RNA-seq was used to characterize the NF-κB transcription factor -mediated regulation of B-cell genome wide target genes upon inducible LMP1 expression . We created an inducible stable EBV-negative Akata Burkitt Lymphoma cell line expressing LMP1 wildtype followed by stable CRISPR knockout of the individual NF-κB transciption factors (p52, RelB, p50, cRel or RelA) and 24 hours 250ng/ml doxycycline-induced LMP1 expression.

2024-01-30 | GSE247495 | GEO

Expression data from Epstein-Barr virus -positive and negative Akata Burkitt's Lymphoma Clones

2010-01-20 | GSE19761 | GEO

Expression data from Epstein-Barr virus -positive and negative Akata Burkitt's Lymphoma Clones

Project description:Transition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV. Keywords: Disease state analysis We used Affymetrix microarrays to examine variations in global gene expression between the paired EBV-positive (1B6) and EBV-negative (2A8) Akata Burkitt's lymphoma clones. EBV-negative Akata clones were generated by treatment with hydroxyurea, an inhibitor of ribonucleotide reductase that forced rapid loss of EBV episomes and compared to their EBV-positive counterparts. Logarithmically growing EBV-negative and positive Akata EBV clones were seeded at 2.5x10^5 cells/ml in RPMI1640 supplemented with 10% fetal bovine serum, 2mM glutamine, and 100units/ml penicillin/streptomycin. The next day, the cells were incubated for 4 hours in media containing 1% fetal bovine serum (low serum), 2mM glutatmine and 100units/ml penicillin/streptomycin to begin selection of the Akata tumor phenotype. The short incubation time was intended to minimize cell death and other potential downstream effects of low serum treatment, while at the same time initiating expression changes contributing to the tumorigenic phenotype.

2010-01-19 | E-GEOD-19761 | biostudies-arrayexpress

Transcriptome analysis of P3HR-1 cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs and Akata EBV+ cells expressing control or myc sgRNAs

Project description:To gain insights into how EBV latency is maintained, we performed a human genome-wide CRISPR screen in latently EBV-infected Burkitt lymphoma B-cells. Our analyses identified a network of host factors that repress EBV lytic reactivation, centered on the transcription factor MYC and including cohesins, FACT, STAGA and Mediator. RNAseq was used to identify host and viral transcriptome changes in P3HR-1 Burkitt lymphoma cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs. RNAseq was used to identify host and viral transcriptome changes in Akata EBV+ burkitt lymphoma cells expressing control or myc sgRNAs.

2020-04-20 | GSE140651 | GEO

Expression data from Burkitt Lymphoma cell lines followed by expression or inhibition of ebv-BART6-3p microRNA

Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines. In order to determine the BART6-3p targets, EBV-negative Akata 2A8 or EBV-positive Akata cells were transiently transfected (in duplicates) with synthetic BART6-3p mimic or inhibitor (100 nM; Custom synthesized by Dharmacon- Thermo Scientific, Germany), respectively. For each treatment, a further transfection with corresponding negative control was performed as well (10 nM; I-300145-01, Dharmacon- Thermo Scientific, Germany). The transfection of 5,000,000 cells per treatment was performed by Amaxa nucleofector apparatus (Amaxa, Cologne-Germany), using the program G23 and the transfection solution V according to the manufacturerâs instructions. Transfection efficiency was assessed by means of a further treatment (2Âµg of pmaxGFP) and detection of both fluorescence and cell viability by flow cytometry. Twenty four hours post-transfection, cells were harvested and RNA was extracted using Trizol, and transfection efficiency was further confirmed by evaluating the expression level of BART6-3p using q-PCR by means of Taqman probes, employing RNU43 as housekeeping miRNA (Applied Biosystems, Cologne, Germany). RNA was further hybridized to HuGene-2.0-st array (Affymetrix, Santa Clara, CA) according to the manufacturer's instructions.

2016-03-02 | E-GEOD-63665 | biostudies-arrayexpress

Gene expression in EBV-positive versus EBV-loss clones derived from endemic Burkitt lymphoma cell lines

Project description:Whilst the association of Epstein-Barr virus (EBV) with Burkitt lymphoma (BL) has long been recognized, the precise role of the virus in BL pathogenesis is not fully resolved. EBV can be lost spontaneously from some BL cell lines, and these EBV-loss lymphoma cells reportedly have a survival disadvantage. We have generated an extensive panel of EBV-loss clones from multiple BL backgrounds and examined their phenotype comparing them to their isogenic EBV-positive counterparts. Whilst loss of EBV from BL cells is rare, it is consistently associated with an enhanced predisposition to undergo apoptosis and reduced tumorigenicity in vivo. We investigated whether there were common gene expression changes between EBV-positive and loss clones derived for four endemic Burkitt lyphoma cell lines that could explain the apoptosis sensitivity of clones that had lost EBV.

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Transcriptomic analysis of LMP1 TES domain single or double mutant in EBV-negative Akata Burkitt Lymphoma Cells

Project description:Transcriptomic analysis of LMP1 TES domain single or double mutant in EBV-negative Akata Burkitt Lymphoma Cells

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circRNA microarray of the Epstein-Barr virus positive Burkitt's lymphoma cell line Akata

Project description:Epstein-Barr virus positive Burkitt's lymphoma cell line Akata (+) and it's EBV-depleted subclone Akata (-) were analyzed for human circRNA expression.

2022-12-19 | GSE206824 | GEO

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