Project description:In this study, approximately 36 and 29 million raw reads of two samples, namely radiation treated strain and its untreated control, are acquired from the sequencing platform. And 143 genes are screened out with the differential expression (DE) analysis.
Project description:Transcriptional profiling of untreated ovarian cancer cells and ovarian cancer cells miR-506 transfected with 48hours. Two-condition experiment, control vs. miR-506 treated cells. One replicate per array.
Project description:In this study, approximately 36 and 29 million raw reads of two samples, namely radiation treated strain and its untreated control, are acquired from the sequencing platform. And 143 genes are screened out with the differential expression (DE) analysis. Investigation of the differential expression between the radiation reduced sample and the wild-type sample in control.
Project description:Purpose: To evaluate whether the single nucleotide polimorphsim rs41291957, located in the pri-miR-143/145, influences the primary RNA secondary structure. Methods: In vitro transcription and folding for the pri-miR-143/145 carrying the WT allele (G) or the mutated one (A) was carried out. The RNAs were then subjected to RNAseI treatement for 30 minutes and RNA seq performed on the digested nucleic acids. Results: Using an optimized data analysis workflow for small RNAs, we mapped the sequence reads on the human pri-miR-143/145 carrying the G- or A-allele. We observed an increase of small reads (<60bps) for the A-allele and a different profile of read enrichement between the digested G- and A-allele RNA, indicating the difference in secondary structure.
Project description:The goal of this experiment was to determine gene expression changes during IFNα treatment as the result of expression or inhibition of miR-203 in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, IFNα treated, IFNα treated in the presence of exogenous miR-203, and IFNα treated in the presence of miR-203 inhibitor) with 3 biological replicates for each group. Total RNA was purified from A549 cells that were untreated of treated with IFNα (1000 units/mL) alone or in the presence of miR-203 mimic or inhibitor for 10 hours.
Project description:To assess the transcriptomic response associated with upregulation of the miR-143/-145 cluster, BRAFV600E mutant human melanoma cells M238P cells were transduced for stable expression of miR-143/145 cluster or with a control vector. Forty-eight hours after transduction, cells were treated with 1 μg/mL of puromycin for one week. RNA samples were then harvested. Two independent experiments were carried out.
Project description:Purpose: To ensure that ABX464 acted specifically on HIV splicing and did not significantly or globally affect the splicing events of human genes, we used a high-throughput RNAseq approach. Many genome-wide expression studies of HIV infection are based on analyses of total peripheral blood mononuclear cells (PBMCs), which consist of over a dozen cell subsets, including T cells, B cells, NK cells and monocytes Methods: The CD4 T cells were uninfected or infected with the YU2 strain and were untreated or treated for 6 days with ABX464, followed by high-throughput RNAseq. Each raw dataset of the samples contained between 44 and 105 million single-end reads (50 bp), with an average of approximately 60 million raw reads per sample Results: Approximately 98% of the total raw reads were mapped to the human genome sequence (GRCh38), giving an average of 60 million human reads per sample for further analyses. The reads that were correctly mapped (approximately 98% of total input reads) to the gene and transcript locations (GTF annotation file) Conclusions: The MDS of our gene expression data showed, without any outliers, that the different donors segregated well and distributed into the DMSO (untreated) and ABX464 treatments that were infected or uninfected. The displayed variance was donor-dependent (clustered by donor) but treatment-independent (no data structure related to the different treatments), which suggests that the ABX464 molecule did not induce a major difference in CD4 T cell gene expression.
