Project description:This SuperSeries is composed of the following subset Series: GSE26877: Nprl3 is Required for Normal Development of the Cardiovascular System GSE27918: Genome-wide maps of chromatin state in mouse erythroid cells. GSE27919: Genome-wide map of DNaseI hypersensitivity in mouse erythroid cells. GSE27920: Transcriptiome of mouse erythroid cells (part2) Refer to individual Series
Project description:Analysis of MDA-MB-231 cells following TSA treatment or not. TSA regulates various miRNA expression in MDA-MB-231 cells.Results provide insight into the role of miRNAs-involved mechanisms underlying TSA-mediated effects on breast cancer stemness.
Project description:To explore how TSA-MSCexo improves myocardial ischemia-reperfusion injury, miRNA microarray analysis was used to screen differentially expressed miRNAs in MSCexo and TSA-MSCexo.
Project description:Endothelial progenitors represent one of the most promising cell-based strategies for vascular repair of ischemic tissue damage, including limb ischemia, myocardial infarction and stroke. We have shown that the transcription factor TAL1 regulates a transcription program that drives the migration and adhesion of ECFCs. Furthermore, treatment of ECFCs with the HDAC inhibitor TSA increases the expression of TAL1-dependent genes and promotes the migration, chemotaxis and adhesion of ECFCs. Finally, ex vivo treatment with TSA also improves the vascular repair properties of ECFCs in vivo when these cells are transplanted in a mouse model of hindlimb ischemia. The goal of this experiment was to test whether TSA treatment of ECFCs affect TAL1 genomic binding. TAL1 ChIP-sequencing was performed from ECFCs that have been treated or not TSA. As negative controls, we performed Mock-ChIP-seq from the same samples using normal IgG instead of the TAL1 antibody. Overall, we find that there is no change in TAL1 genomic binding in ECFCs upon TSA treatment.
Project description:In order to identify the TSA responsive genes, we performed a gene expression microarray analysis for the RNAs isolated from TSA-untreated and TSA-treated human keratinocytes
Project description:ngs2012_02_microd-ngs microd-part2-Effect of dilution on RNA seq sensitivity-One sample of total RNA extracted from whole embryo by laser assisted microdissection was diluted from 5ng to 10pg to check sensitivity of the library construction and subsequent sensitivity of transcript identification by RNA seq.
Project description:To explore TSA influence on human breast cancer cells, we attempt to analyze genes differentially expressed between TSA treated and untreated SKBR3 cells, which will hopefully provide clues for TSA target genes.
Project description:An investigation of gene expression changes in rectal biopsies from donors with IBS compared to controls to begin to understand this complex syndrome. To further investigate differences between IBS groups (constipation and diarrhoea predominant) (part1) and how IBS relates to bacterial infection (part2) with biopsies taken 6 months after Campylobacter jejuni infection. Part1: 18 Constipation predominant IBS subjects (IBS-C) and 27 diarrhoea predominant IBS subjects (IBS-D) compared to 21 healthy volunteers (HV). Part2: 21 Campylobacter jejuni infection (PIBD, PIBS, PINIBS) compared to 19 healthy volunteers (HV). PIBD = post Campylobacter infection with IBS (within 6 months) PIBS = post infection IBS (unknown time point and organism) PINIBS = post Campylobacter infection with no resulting IBS
Project description:Treatment with the histone deacetylase inhibitor trichostatin a (TSA) changes the radial positioning of the CFTR gene in HeLa S3 cells. The gene relocates from the nuclear periphery to the nuclear interior. In Calu-3 cells the gene is located in the nuclear interior. To identifiy potential regulatory elements for the positioning of CFTR, the histone h3 and h4 acetylation patterns of untreated and TSA-treated HeLa S3 and untreated Calu-3 cells were determined by ChIP-chip. A CTCF site close to the CFTR promoter displayed consistent histone H3 hyperacetylation in TSA treated HeLa S3 cells and Calu-3 cells.
Project description:These data were used for prediction of neoantigens and minor histocompatibility mismatch antigens, which were subsequently used for design of a machine-learning algorithm for tumor-specific antigen (TSA) immunogenicity prediction. TSA vaccines are a growing area of study for cancer immunotherapy, but identification of clinically relevant targets remains a challenge. The study associated with these data provides the first description of a computational method for direct prediction of TSA immunogenicity trained entirely from validated TSA immunogenicity scores. This tool has allowed us to 1) predict for clinically efficacious TSA targets, 2) identify genomic correlates of TSA immunogenicity, and 3) demonstrate evidence of alternative out-of-frame TSAs which can promote anti-tumor immunity.
