Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex
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ABSTRACT:
PROVIDER: PRJNA796615 | ENA |
REPOSITORIES: ENA
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Project description:HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on splicing patterns in CEM cells by exon microarray analysis.
2022-03-03 | GSE193574 | GEO
Project description:HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on gene expression profiles in CEM cells by gene expression microarray analysis.
2022-03-03 | GSE193576 | GEO
Project description:Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex
| PRJNA796617 | ENA
Project description:Human T-cell leukemia virus type 1 (HTLV-1) is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax oncoprotein regulates viral gene expression and the NF-kB pathway to promote the survival of HTLV-1 infected T cells. In thsi study, we utilize a kinome-wide shRNA screen to identify the tyrosine kinase KDR/VEGFR2 as an essential survival factor of HTLV-1-transformed T cells. Inhibition of KDR induces apoptosis of Tax expressing HTLV-1-transformed cell lines and CD4+ T cells from HAM/TSP patients. Phosphoproteomics analysis of HTLV-1 transformed cells treated with a KDR inhibitor revealed inhibition of the phosphorylation of multiple receptors/cell surface proteins, ubiquitin conjugating systems, proteases, phosphatases, apoptotic regulatory factors, adhesion/extracellular matrix proteins and viral proteins. This work suggests that HTLV-1 Tax has hijacked KDR kinase activity to promote Tax stability and the proliferation and survival of HTLV-1 infected cells.
2024-06-14 | PXD051981 | Pride
Project description:A conditional and isogenic system for APOBEC3B (A3B) induction in T-REx-293 cells. Cells were engineered to express doxycycline-inducible A3B-eGFP or eGFP constructs and subjected to 10 rounds of A3B-eGFP exposure causing 80-90% cell death. Control pools (eGFP) were subjected to parallel rounds of non-toxic eGFP exposure, and dilutions were done each round to mimic A3B-eGFP induced population fluctuations. DNA was extracted and subjected to SNP analyses using the Human OmniExpress-24v1-0 BeadChip (Illumina, San Diego, CA). Genotyping was performed using the humanomniexpress_24v1-0_a cluster file.
2016-06-30 | GSE78710 | GEO
Project description:The objective of this comparison was to identify the impact of rex deletion on the transcriptome of Streptococcus pneumoniae D39. This comparison showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. In this study, we investigated the transcriptomic response of Streptococcus pneumoniae D39 to NADH. Transcriptome comparison of the D39 wild-type grown in chemically-defined medium (CDM) with 0 mg/ml NADH to 0.5 mg/ml NADH revealed elevated expression of various genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in the transport and biosynthesis of niacin. Microarray results were further confirmed by β-galactosidase assays. Promoter-lacZ fusions assays and microarray studies showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. The putative operator site of Rex in the promoter regions of Rex-regulated genes is predicted and confirmed by promoter mutational experiments.
2018-06-01 | GSE94571 | GEO