E-MTAB-5112
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5112 | ExpressionAtlas | 2016-12-15
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Sequencing the transcriptome of DBAxC57BL/6J mice. To study the regulation of transcription, splicing and RNA turnover we have sequenced the transcriptomes of tissues collected DBAxC57BL/6J mice. We strongly encourage researchers to contact us if there is any queries about referencing or publishing analysis based on pre-publication data. This data is part of a pre-publication release. For information on use of the data and the data release policy please see: http://www.sanger.ac.uk/resources/mouse/genomes/datarelease.html ArrayExpress Release Date: 2011-04-09 Publication Title: Sequence variation amongst 17 classical and wild-derived mouse genomes and its effect on gene regulation and phenotypic variation. Publication Author List: Thomas M. Keane, Petr Daneck, Leo Goodstadt, Bret Payseur, Michael White, Kim Wong, Binnaz Yalcin, Andreas Heger, Avi Agam, Guy Slater, Martin Goodson, Nick Furotte, Eleazar Eskin, Christoffer Nellaker, Helen Whitley, James Cleak, Deborah Janowitz, Polinka Hernandez-Pliego, Amartjit Bhomra, Jerome Nicod, Xiangchao Gan, Wei Yuan, Louise van der Weyden, Sendu Bala, Allan Bradley, Jim Stalker, Richard Mott, Richard Durbin, Ian Jackson, Laura Reinholdt, Chris P. Ponting, Ewan Birney, Jonathan Flint, David J. Adams Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute Person Roles: project owner Person Last Name: Adams Person First Name: David Person Mid Initials: Person Email: da1@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30617 | GEO
Project description: Not available
| S-BSST1361 | biostudies-other
Project description:Transcriptome sequencing of E.coli K12 in LB media in early exponential phase and transition to stationary phase ArrayExpress Release Date: 2010-09-30 Person Roles: submitter Person Last Name: Martincorena Person First Name: Inigo Person Mid Initials: Person Email: martinco@ebi.ac.uk Person Phone: Person Address: Person Affiliation: EBI
2011-02-05 | GSE24998 | GEO
Project description:Raw data from E-MTAB-1585 was normalized by using reads per million. https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1585/ Strand specific RNA-Seq data E-MTAB-1585 was normalized and subtracted control from knockdown to generate tracks that more clearly displayed the unusual pattern of RNA expression caused by knockdown of 7SK. The following wig files were generated from multiple samples (i.e.raw data files), as indicated in the 'readme.txt' file. 7sk_3p_KD_norm.wig: 7SK 3P Knockdown normalized 7sk_3p_KDF_norm.wig: 7SK 3P Knockdown normalized (Forward) 7sk_3p_KDR_norm.wig: 7SK 3P Knockdown normalized (Reverse) 7sk_5p_KD_norm.wig: 7SK 5P Knockdown normalized 7sk_5p_KDF_norm.wig: 7SK 5P Knockdown normalized (Forward) 7sk_5p_KDR_norm.wig: 7SK 5P Knockdown normalized (Reverse) 7sk_Control_norm.wig: 7SK Control normalized 7sk_ControlF_norm.wig: 7SK Control normalized (Forward) 7sk_ControlR_norm.wig: 7SK Control normalized (Reverse) 7sk_3p_KDF-ControlF.wig: 7SK 3P Knockdown-Control (Forward) 7sk_3p_KDR-ControlR.wig: 7SK 3P Knockdown-Control (Reverse) 7sk_5p_KDF-ControlF.wig: 7SK 5P Knockdown-Control (Forward) 7sk_5p_KDR-ControlR.wig: 7SK 5P Knockdown-Control (Reverse)
2013-09-19 | E-GEOD-50860 | biostudies-arrayexpress
Project description:Recent advances in high throughput sequencing methodologies allow the opportunity to probe in depth the transcriptomes of organisms including N. caninum. In this project, we are using Illumina sequencing technology to analyze the transcriptome (RNA-Seq) of experimentally accessible stages (e.g. tachyzoites at different times points) of N. caninum NCLiv. The aim is to make transcriptional landscape maps at different time points at different life cycle stages of N. caninum and compare it with equivalent datasets from the closely related parasite Toxoplasma gondii. ArrayExpress Release Date: 2011-02-08 Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute Person Roles: Investigator Person Last Name: Reid Person First Name: Adam Person Mid Initials: Person Email: ar11@sanger.ac.uk Person Phone: 01223 834244 Person Address: Wellcome Trust Genome Campus,Hinxton,Cambridge. CB10 1SA UK Person Affiliation: Wellcome Trust Sanger Institute Person Roles: Project Coordinator Person Last Name: Sanders Person First Name: Mandy Person Mid Initials: J Person Email: mjs@sanger.ac.uk Person Phone: 01223 834244 Person Address: Wellcome Trust Genome Campus,Hinxton,Cambridge. CB10 1SA UK Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30613 | GEO
Project description:Recent advances in high throughput sequencing methodologies allow the opportunity to probe in depth the transcriptomes of organisms including N. caninum and Toxoplasma gondii. In this project, we are using Illumina sequencing technology to analyze the transcriptome (RNA-Seq) of experimentally accessible stages (e.g. tachyzoites at different times points) of T. gondii VEG strain. The aim is to make comparative transcriptional landscape maps of Neospora and Toxoplasma at different time points at different life cycle stages and compare levels of expression of orthologous genes in these two organisms. ArrayExpress Release Date: 2011-02-08 Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute Person Roles: Investigator Person Last Name: Reid Person First Name: Adam Person Mid Initials: Person Email: ar11@sanger.ac.uk Person Phone: 01223 834244 Person Address: Wellcome Trust Genome Campus,Hinxton,Cambridge. CB10 1SA UK Person Affiliation: Wellcome Trust Sanger Institute Person Roles: Project Coordinator Person Last Name: Sanders Person First Name: Mandy Person Mid Initials: J Person Email: mjs@sanger.ac.uk Person Phone: 01223 834244 Person Address: Wellcome Trust Genome Campus,Hinxton,Cambridge. CB10 1SA UK Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30614 | GEO
Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.
2022-07-27 | GSE158191 | GEO
Project description:Accurate and comprehensive de novo transcriptome profiling in heart is a central issue to better understand cardiac physiology and diseases. Although significant progress has been made in genome-wide profiling for quantitative changes in cardiac gene expression, current knowledge offers limited insights to the total complexity in cardiac transcriptome at individual exon level. To develop more robust bioinformatic approaches to analyze high-throughput RNA sequencing (RNA-Seq) data, with the focus on the investigation of transcriptome complexity at individual exon and transcript levels. In addition to overall gene expression analysis, the methods developed in this study were used to analyze RNA-Seq data with respect to individual transcript isoforms, novel spliced exons, novel alternative terminal exons, novel transcript clusters (i.e., novel genes) and long non-coding RNA genes. We applied these approaches to RNA-Seq data obtained from mouse hearts following pressure-overload induced by trans-aortic constriction. Based on experimental validations, analyses of the features of the identified exons/transcripts, and expression analyses including previously published RNA-Seq data, we demonstrate that the methods are highly effective in detecting and quantifying individual exons and transcripts. Novel insights inferred from the examined aspects of the cardiac transcriptome open ways to further experimental investigations. Our work provided a comprehensive set of methods to analyze mouse cardiac transcriptome complexity at individual exon and transcript levels. Applications of the methods may infer important new insights to gene regulation in normal and disease hearts in terms of exon utilization and potential involvement of novel components of cardiac transcriptome. Left ventricular tissues were collected from C57BL/6 mice after 1 week (hypertrophy stage, HY) and 8 weeks post trans-aortic constriction (TAC) procedure (heart failure stage, HF), respectively, and their corresponding Sham controls (Sham-HY, Sham-HF). To conduct RNA-Seq analysis, total RNAs from six TAC and Sham-operated mice at the HY stage and four TAC and corresponding Sham mice at the HF stage were obtained.
2011-10-18 | E-GEOD-29446 | biostudies-arrayexpress
Project description:Illumina bodyMap2 transcriptome Transcription profiling by high throughput sequencing of individual and mixture of 16 human tissues RNA. Additional supplementary files available at foot of this record. Additional information available as supplementary files at the foot of this record. ArrayExpress Release Date: 2011-03-17 Person Roles: submitter Person Last Name: Khrebtukova Person First Name: Irina Person Mid Initials: Person Email: ikhrebtukova@illumina.com Person Phone: 1-510-723-9219 Person Address: 25861 Industrial Blvd, Hayward CA 94545, USA Person Affiliation: Illumina
2011-07-14 | GSE30611 | GEO
Project description:Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. α1-ARs and β-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes. However, little is known about the functional similarities and differences between α1- and β-ARs activated temporal responses in stress-induced cardiac pathology. In this work, we systematically compared the cardiac temporal genome-wide profiles of acute α1-AR and β-AR activation in the mice model by integrating transcriptome and proteome. We found that α1- and β-AR activations induced sustained and transient inflammatory gene expression, respectively. Particularly, the overactivation of α1-AR but not β-AR led to neutrophil infiltration at 1 day, which was closely associated with the up-regulation of chemokines, activation of NF-κB pathway, and sustained inflammatory response. Furthermore, there are more metabolic disorders under α1-AR overactivation compared with β-AR overactivation. These findings provide a new therapeutic strategy that besides using β-blocker as soon as possible, blocking α1-AR within one day should also be considered in the treatment of acute stress associated cardiovascular diseases.
2023-01-19 | PXD036011 | Pride