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.

2018-01-25 | GSE100458 | GEO

Apoptosis-associated transcriptome changes in peripheral blood leukocytes during CMV antiviral therapy

Project description:refer to the SuperSeries

2018-01-31 | GSE109959 | GEO

Proteomics Deciphering the Underlying Mechanism of Tgfb1 Regulating Dendritic Cells

Project description:In current study, we conducted a lentivirus-based overexpression system and observed that overexpressing Tgfb1 successfully promoted the viability and altered the cell cycle distribution in DC. What’s more, this gene also greatly inhibited apoptosis of DC, highlighting the robust immune support effects of Tgfb1 function. Additionally, a quantitative proteomic was implemented to explore the underlying mechanism. Comparing Tgfb1 overexpressed (OE) and normal control (NC) groups, numerous differentially expressed proteins (DEPs) were emerged, which contributed to this phenomenon. Finally, bioinformatics analysis revealed multiple DEPs enriched in immune-related pathways directly or in a roundabout way, which manifested the crucial role played by Tgfb1 in DC.

2021-09-23 | PXD028716 |

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