Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169564 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profile of splenic B cells (CD19+) from transgenic mice expressing the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and/or LMP2A. Freshly harvested primary B cells were profiled. B lymphocytes from transgenic LMP1, LMP2A, LMP1/2A mice and negative littermates were profiled from 6 month old adult mice; lymphoma cells were passaged in SCID mice and profiled for three LMP1 positive lymphomas and one negative lymphoma.
2012-09-01 | GSE38954 | GEO
Project description:Gene expression profile of splenic B cells (CD19+) from transgenic mice expressing the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and/or LMP2A. Freshly harvested primary B cells were profiled. B lymphocytes from transgenic LMP1, LMP2A, LMP1/2A mice and negative littermates were profiled from 6 month old adult mice; lymphoma cells were passaged in SCID mice and profiled for three LMP1 positive lymphomas and one negative lymphoma. 12 total samples. 4 transgenic B lymphocyte samples pooled from multiple biological replicates were hybridized to duplicate microarrays: LMP1 (pooled from 2 replicates), LMP2A (pooled from 3 replicates); LMP1/2A (pooled from 5 replicates), negative littermates (pooled from 4 replicates). 3 biological replicates of LMP1 lymphomas expressing high, medium and low levels of LMP1 and; 1 negative lymphoma was hybridized to 1 microarray chip. The reference sample consisted of 4 biological replicates of splenic B cells (CD19+) pooled from 4-7 month old non-transgenic Balb/c mice. The same reference was used for all hybridizations.
2012-09-01 | E-GEOD-38954 | biostudies-arrayexpress
Project description:Epstein-Barr virus has been reported to regulate cellular microRNA expression in B cells. In the present study, we investigated the differential microRNAs modulated by Epstein-Barr virus in Naspharyngeal Carcinoma, using CapitalBio corporation's mammalian miRNA arrays. Three cellular models were used in this study: the human naspharyngeal carcinoma cell line TW03 as a blank control; TW03 transfected with Epstein-Barr virus encoded LMP1; TW03 transfected with Epstein-Barr virus encoded LMP2A
2011-01-13 | E-GEOD-26596 | biostudies-arrayexpress
Project description:Comparsion of cellular gene expression between a control B lymphoma cell-line (BJAB pz2) stably transfected with an empty vector and a BJAB cell-line stably expressing Epstein-Barr virus EBNA 3C (BJAB E3C-4). These cell lines are described in Wang, F., C. Gregory, C. Sample, M. Rowe, D. Liebowitz, R. Murray, A. Rickinson, and E. Kieff. 1990. Epstein-Barr virus latent membrane protein (LMP1) and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymphocytes: EBNA-2 and LMP1 cooperatively induce CD23. J Virol 64:2309-2318)
2012-03-13 | E-MEXP-3585 | biostudies-arrayexpress
Project description:Analysis of gene expression profiling change by expression of Epstein-Barr virus latent membrane protein 2A (LMP2A) in B cells
2015-07-07 | GSE70521 | GEO
Project description:A Mouse Model of Epstein-Barr virus LMP1 and LMP2A Driven Germinal Center B-cell Lymphoproliferative Disease
| PRJNA362541 | ENA
Project description:We have developed a transgenic mouse model for Epstein-Barr virus-associated Burkitt's lymphoma. Transgenic mice that express LMP2A and MYC in B cells develop spontaneous lymph node tumors at different rates. Tumor onset occurs at approximately 40-60 days in LMP2A/λ-MYC mice and at 100-200 days in λ-MYC mice. This study compared total gene expression in the tumor cells from each genotype, as well as in B cells isolated from 3 week old mice prior to tumor onset. Comparison of total gene expression in tumor cells from LMP2A/λ-MYC and λ-MYC transgenic mice identified a short list of differentially expressed genes. Comparison of gene expression in B cells from the spleens of 3 week old mice, in contrast, identified a 10-fold increase in the number of differentially expressed genes.
2011-10-26 | GSE26918 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE10057: The Epstein-Barr Virus latent membrane protein 1 (LMP1) induces cellular microRNA146a GSE10105: Alteration of microRNA gene expression by EBV encoded LMP1 oncogene Keywords: SuperSeries Refer to individual Series
2008-01-08 | E-GEOD-10107 | biostudies-arrayexpress
Project description:Analysis of gene expression profiling change by expression of Epstein-Barr virus latent membrane protein 1 (LMP1) in B cells
2018-08-24 | GSE93966 | GEO
Project description:Epstein-Barr virus (EBV) infects human B cells and reprograms them to allow virus replication and persistence. One key viral factor in this process is latent membrane protein 2A (LMP2A), which has been described as a B cell receptor (BCR) mimic promoting malignant transformation. However, how LMP2A signaling contributes to tumorigenesis remains elusive. By systematically comparing LMP2A and BCR signaling using quantitative phosphoproteomics and transcriptome profiling, we identified molecular mechanisms through which LMP2A affects B cell biology. Consistent with previous literature, we found that LMP2A mimics a subset of BCR signaling events, including tyrosine-phosphorylation of the kinase SYK, the calcium initiation complex consisting of BLNK, BTK, PLC2, and its downstream transcription factor NFAT. However, the vast majority of LMP2A-induced signaling events markedly differed from those induced by BCR stimulation. These included differential phosphorylation of kinases, phosphatases, adaptor proteins, transcription factors such as NFB and TCF3, as well as widespread changes in the transcriptional output of LMP2A-expressing B cells. LMP2A affected apoptosis and cell cycle checkpoints by dysregulating the expression of apoptosis regulators such as Bcl-xL and the tumor suppressor retinoblastoma-associated protein (RB1). Accordingly, LMP2A cooperated with drivers of Burkitt lymphoma, overexpressed MYC and an oncogenic cyclin D3 mutant, by counteracting the pro-apoptotic effects of MYC and by further inhibiting RB1 function to promote cell growth. Our results indicate that LMP2A rewires rather than mimics BCR signaling, promoting a signaling output that predisposes EBV-infected B cells to hyperproliferation and eventual malignant transformation.
2020-09-22 | PXD018566 | Pride