M6A mapping in mouse RNA (mouse liver and human brain)
Ontology highlight
ABSTRACT: We developed a novel approach, m6A-seq, for high-resolution mapping of the transcriptome-wide m6A landscape, based on antibody-mediated capture followed by massively parallel sequencing Identification of m6A modified sequences in mouse liver and human brain
Project description:This SuperSeries is composed of the following subset Series: GSE36958: Gene expression profiles of WT and ime4-/- mutant yeast cells, under vegetative and meiosis-inducing conditions GSE37001: METTL3 KD in HepG2 cells GSE37002: m6A mapping in human RNA (with treatments) GSE37003: m6A mapping in human RNA (untreated) GSE37004: m6A mapping in mouse RNA (mouse liver and human brain) Refer to individual Series
Project description:We developed a novel approach, m6A-seq, for high-resolution mapping of the transcriptome-wide m6A landscape, based on antibody-mediated capture followed by massively parallel sequencing. Identification of m6A modified sequences in HepG2 cells.
Project description:We developed a novel approach, m6A-seq, for high-resolution mapping of the transcriptome-wide m6A landscape, based on antibody-mediated capture followed by massively parallel sequencing. Identification of m6A modified sequences in HepG2 cells. HepG2 cells were incubated with either IFNg (200ng/ml) or HGF/SF (10 ng/ml) over night. Stress effects were tested in HepG2 cells by either 30 minutes incubation at 43M-BM-:C (heat shock) or UV irradiation of 0.04 J/cm2 followed by 4 hours of recovery in normal growing conditions prior to harvesting using Trypsin.
Project description:p63 is a transcription factor central for epithelial homeostasis and development. In our model of epithelial to mesenchymal transition (EMT) in a human prostate cell culture model, p63 was one of the most down-regulated transcription factors during EMT. We therefore investigated the role of p63 in EMT by a gain and loss of function approach. Over-expression of the predominant epithelial isoform DNp63a in mesenchymal EPT1B8 cells led to gain of several epithelial characteristics without resulting in a complete mesenchymal to epithelial transition (MET). This was corroborated by a reciprocal effect when p63 was knocked down in epithelial EP156T cells. Global gene expression analyses found that DNp63a induced gene modules involving cell adhesion genes in mesenchymal like cells. Genome-wide analysis of p63 binding sites by ChIP-seq analyses confirmed binding of p63 to regulatory areas of genes associated with cell adhesion in prostate epithelial cells.CDH1 and ZEB1 are two elemental factors in the control of EMT. Over-expression and knock-down of these factors, respectively, were not sufficient alone or in combination with DNp63a to reverse the mesenchymal phenotype in EPT1 cells. The partial reversion of epithelial to mesenchymal transition might reflect the ability of DNp63a, as a key co-ordinator of several epithelial gene expression modules, to reduce epithelial to mesenchymal plasticity (EMP). The utility of DNp63a expression and the potential of reduced EMP in order to counteract metastasis warrant further investigation. Examination of p63 binding profile in prostate cell model EP156T with EPT1 as negative control.
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of H3K4me3 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle
Project description:In this study we have examine the deposition of H3K4me1,H3K4Me3 and H3K27Ac and the Nodal transcription factor, Smad2/3, immediately following zygotic transcription and continuing through gastrulation. We profiled 4 histone modifications (H3K4Me3, H3K27Me3, H3K27AC, H3K4Me1) and one transcription factor smad2/3 (+ chromatin input) using ChIP-Seq, and expression profiles (3' RNA-Seq) for Xenopus tropicalis embryos stage8, stage9 and stage10.5. Furthermore, we have profile two histone modifications (H3K4Me1 and H3K27Ac) in absance of nodal signaling in stage9 Xenopus tropicalis embryos using ChIP-seq and 3-seq
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated withionizing radiation ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with ionizing radiation or vehicle
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a MDM2 inhibitor nutlin-3 ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with nutlin-3 or vehicle
Project description:Temporal analysis of Irf4 and PU.1 genome binding during B cell activation and differentiation in vitro using antigen (NP-Ficoll) CD40L and IL-2/4/5 cytokines (see Molecular Systems Biology 7:495 for details of cellular system). The results provide insight in the target genes and binding specificity of IRF4 and PU.1 during coordination of different programs of B cell differentiation. Regrettably three of the FASTQ raw sequence files in our study were corrupted during storage. FASTQ data from our experimental and control groups are available for download via GEO SRA; however, two groups are missing select raw sequence files. These include one PU.1 Day 3 group file (Sample GSM1133499) and two of four input files used to generate a concatenated “super” input file (Sample GSM1133490); the raw data provided for input consists of the two input files recovered. Importantly, FASTA sequences for both of these datasets are available as supplementary data through GEO, and we can make available upon request (rsciamma@uchicago.edu) all files in our study in the ELAND-extended alignment format. Please note that GEO no longer supports this format. Resting mature peripheral primary B cells were enriched from the spleens of B1-8i (anti-NP gene targeted) mice. We sought to compare the genome-binding landscape of Irf4 and PU.1 prior to differentiation yet after B cell activation (Day 1) and after B cell differentiation (Day 3) of activated B cells into plasma cells (see Molecular Systems Biology 7:495 for description of cellular system). To this end, we used ChIP-seq (using the Illumina GA2 system) to obtain millions of unbiased, genome-wide, binding events. Sequences were mapped to the reference genome (mm9) and enrichment was calculated, relative to an Input sample, using QuEST algorithms.