Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1288484 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the effect of a particular gene on CVA6 replication, we established a CVA6-infected RD cell line. We then performed gene expression analysis using RNA-seq data of cells from the infected and uninfected groups.
2023-03-30 | GSE227507 | GEO
Project description:IgG4-related disease (IgG4-RD) is an autoimmune disease with an unknown etiology. In this study, we focused on non-hematopoietic cells in the submandibular gland of IgG4-RD patients. Through single-cell RNA sequencing, our aim was to unravel the contributions of these cells to the development and progression of IgG4-RD.
2024-02-19 | GSE242778 | GEO
Project description:Among the non-polio enterovirus (NPEV) Echovirus-30 (E-30) is responsible for extensive global outbreaks of meningitis in children. To gain access to the central nervous system (CNS), E-30 first have to cross one of the two main barriers, the epithelial blood-cerebrospinal fluid (CSF) barrier (BCSFB) or the endothelial blood-brain barrier (BBB). Previously it has been shown that several meningitis causing bacteria preferentially infect human choroid plexus papilloma cells (HIBCPP) in a polar fashion from the basolateral cell side. Here, we investigated the polar infection with E-30 of HIBCPP cells. Both, apical and basolateral infections caused a significant decrease of the transepithelial resistance (TEER) of HIBCPP cells in a dose-dependent manner. However, to reach the same TEER decrease the multiplicity of infection (MOI) of the apical infection had to be 20 times higher than the basolateral infection. In line with this finding the number of infected cells at respective time-points after basolateral infection was significantly higher compared to apical infection. Cytotoxic effects of E-30 on HIBCPP cells during basolateral infection were observed following prolonged infection, and appeared more drastically compared to the apical infection. Evaluation of massive analysis of cDNA ends (MACE) RNA data comparing basolateral versus apical infection, revealed a distinct pattern of up- and down-regulated genes depending on the side of infection. Especially, the down-regulation of ITGα5 upon basolateral infection can be correlated with a more drastic impact of E-30 on the HIBCPP cells when compared to apical infection, leading to structural changes. Also, type 3 interferon genes might be a factor involved in the polar effect of E-30 on HIBCPP. Altogether, the data highlights the polar effect of E-30 in HIBCPP cells as an important factor for an efficient infection.
2020-10-02 | GSE146890 | GEO
Project description:Rhabdomyosarcoma is a pediatric tumor of skeletal muscle that expresses the myogenic basic helix-loop-helix protein MyoD but fails to undergo terminal differentiation. Prior work has determined that DNA binding by MyoD occurs in the tumor cells, but myogenic targets fail to activate. Using MyoD chromatin immunoprecipitation coupled to high-throughput sequencing and gene expression analysis in both primary human muscle cells and RD rhabdomyosarcoma cells, we demonstrate that MyoD binds in a similar genome-wide pattern in both tumor and normal cells but binds poorly at a subset of myogenic genes that fail to activate in the tumor cells. Binding differences are found both across genomic regions and locally at specific sites that are associated with binding motifs for RUNX1, MEF2C, JDP2, and NFIC. These factors are expressed at lower levels in RD cells than muscle cells and rescue myogenesis when expressed in RD cells. MEF2C is located in a genomic region that exhibits poor MyoD binding in RD cells, whereas JDP2 exhibits local DNA hypermethylation in its promoter in both RD cells and primary tumor samples. These results demonstrate that regional and local silencing of differentiation factors contributes to the differentiation defect in rhabdomyosarcomas. ChIP-Seq profiling of MyoD in human myotube, myoblast and rhabdomyosarcoma cells
2013-08-29 | E-GEOD-50413 | biostudies-arrayexpress
Project description:We report here the analysis of TRPS1 chromatin binding by ChIP-Seq in embryonal rhabdomyosarcoma RD cells. We use here parental and TRPS1-KO RD cells. RD cells and RD-TRPS1-KO cells were cultured in growth medium and chromatin was prepared. TRPS1 DNA binding in RD cells and RD-TRPS1-KO cells using a selfmade antibody (referenced in Elster et al.) was determined by ChIP-seq.
2023-07-24 | GSE197550 | GEO
Project description:Single-cell RNA sequencing (scRNA-seq) data of peripheral blood mononuclear cells (PBMCs) obtained from 30 ATL patients (34 samples including 4 sequential ones), 11 HTLV-1-infected asymptomatic carriers, and 4 healthy donors.
| EGAD00001007015 | EGA
Project description:MicroRNAs are noncoding RNA species comprising 18–23 nucleotides that regulate host-virus interaction networks. Here, we showed that enterovirus A71 infection in human rhabdomyosarcoma (RD) involved miR-197 expression. miR-197 can regulate virus replication in the context of viral RNA synthesis via the transfection of its mimic into RD cells. We employed a mass spectrometry-based quantitative proteomic stable isotope labeling with amino acids in cell culture (SILAC) approach for the identification of miR-197 target genes by transfecting mimetic miR-197 into RD cells, and the differential expression of prospective target proteins was identified. A total of 1,822 genes were repeatedly and considerably downregulated in miR-197-transfected RD cells, 106 of which were predicted to have seed sites by TargetScan. Seven of the selected 8 genes potentially related to viral replication and immune response were confidently validated as direct miR-197 targets using a luciferase (untranslated region (3'-UTR)) reporter assay. The expression of three selected endogenous molecules (ITGAV, ETF1, and MAP2K1 (MEK1)) was significantly reduced when RD cells were transfected with an miR-197 mimic. Our results provide a database of miR-197 targets, which is potentially of interest in the area of viral pathogenesis and other research fields.
2018-10-24 | PXD010585 | Pride