Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of control and Lmna -/- mice heart samples

ABSTRACT: RNA-sequencing analysis from whole heart ribosome depleted RNA from the 2-week old WT and Lmna-/- mice (N=5) . Strand specific RNA seq libraries where prepared form ribosome-depleted cardiac RNA samples using the Illumina TruSeq stranded total RNA library preparation kit. The samples weresequenced on the Illumina HiSeq 4000 instrument using the paired-end sequencing reagents to generate100 base paired end reads.

ORGANISM(S): Mus musculus

PROVIDER: GSE110341 | GEO | 2019/02/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from E161K LMNA mutant heart and control

Project description:Over 180 LMNA gene mutations have been identified in human diseases including cardiac and skeletal myopathies, lipodystrophies, and premature aging syndromes. Postulated mechanisms by which these mutations result in different phenotypes include perturbation of normal nuclear structure and chromosome organization, and gene activity. We investigated whether a cardiomyopathic LMNA mutation, E161K, displayed abnormal gene expression. We compared the gene expression profile in the E161K LMNA-mutant heart to that of an end stage LMNA-normal heart. We compared the gene expression levels between two end-stage cardiomyopathic hearts in order to detect the gene expression differences more likely to reflect the LMNA mutation state. A region of left ventricle tissue that was grossly less fibrotic and contained cardiomyocytes of the LMNA-mutant heart was selected for RNA isolation. A region of a male heart that was also end-stage dilated cardiomyopathy, but LMNA-normal and also devoid of obvious fibrosis was selected for RNA isolation. Two technical replicates were performed for each sample, and data were analyzed using two different normalization strategies (Mas5 and RMA).

2010-01-30 | E-GEOD-17476 | biostudies-arrayexpress

ena-DATASET-DKFZ-11-09-2018-14:03:31:711-448 - samples

Project description:Paired-end, ribosome depleted, total RNA Sequencing

| EGAD00001004327 | EGA

Exercise Reverses Dysregulated Gene Expression in a Desmoplakin Haplo-insufficient Mouse Model of Arrhythmogenic Cardiomyopathy

Project description:Mutations in desmosome genes cause arrhyythmogenic cardiomyopathy (ACM). Using desmoplakin haploinsufficient mouse model of ACM, we evaluated the effects of treadmill exercise on cardiac myocyte transcritional profile. Strand specific, ribosome depleted paired end RNA sequencing of cardiac myocytes from wild type and Myh6-Cre:DspW/F were generate using Illumina HiSeq 4000.

2020-04-29 | GSE129962 | GEO

Expression data from E161K LMNA mutant heart and control

2010-01-30 | GSE17476 | GEO

Gene expression profile in Lmna knockout mouse embryonic fibroblast

Project description:Alteration of gene expression profile due to Lmna knockout was studied in MEF. Total RNA obtained from Lmna +/+ MEF and Lmna -/- MEF were compared.

2012-06-18 | E-GEOD-38777 | biostudies-arrayexpress

Expression data from Head and neck squamous cell carcinoma cell lines cell line Cal27 after TCF19 knockout mediated by CRISPR/CAS9

Project description:The deletion of TCF19 in CAL27,oral squamous cell carcinoma cell line,was conducted by using CRISPR/Cas9 system. For WT and TCF19 KO CAL27 cell lines, samples were done in triplicates. A total of 3μg of high-quality RNA per sample was used for ribosomal RNA removal by the Epicentre Ribo-zero rRNA Removal Kit (Epicentre, USA) and the sequencing library was prepared using the rRNA-depleted RNA by the NEBNext Ultra Directional RNA Library Prep Kit for Illumina (NEB, USA) following manufacturer’s recommendations. The clustering of the index-coded samples was performed on a cBot Cluster Generation System using TruSeq PE Cluster Kit v3-cBot-HS (Illumina, San Diego, CA, USA), followed by the 150-bp paired-end sequencing on the HiSeq X Ten instrument (Illumina, San Diego, CA, USA) according to the manufacturer’s protocols.

2021-01-01 | GSE153354 | GEO

Interplay of stress responses underlying the development of LMNA cardiomyopathy

Project description:Mutations in the LMNA gene encoding nuclear lamins A/C cause a diverse array of tissue-selective diseases, with the heart being the most commonly affected organ. Despite progress in understanding the molecular perturbations emanating from LMNA mutations, an integrative understanding of the pathogenesis leading to cardiac dysfunction remains elusive. Using a novel cell-type specific Lmna deletion mouse model capable of translatome profiling, we found that cardiomyocyte-specific Lmna deletion in adult mice led to rapid cardiomyopathy with pathological remodeling. Prior to the onset of cardiac dysfunction, lamin A/C-depleted cardiomyocytes displayed nuclear envelope deterioration, disruption of the ER-golgi interface, and ER stress. Translatome profiling identified upregulation of Med25, a transcriptional co-factor involved in unfolded protein responses. Culturing Lmna-deleted cardiomyocytes in stiff hydrogels recapitulated these pathological features, confirming that cardiomyocyte-extrinsic factors contribute to the pathogenesis. Pharmacological activation of autophagy or modulation of ER stress significantly improved the cardiac function. These studies support a unified hypothesis wherein cardiomyopathy develops from autophagic impairment that exacerbates ER stress emanating from nuclear envelope deterioration.

2022-10-11 | GSE185620 | GEO

ATAC-seq data from Lmna knock-out mouse embryonic fibroblasts (Lmna-/- MEFs) and wild type (Lmna+/+ MEFs)

Project description:Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.

2022-08-31 | GSE186677 | GEO

peat metagenome

Project description:Illumina MiSeq paired end sequencing

| PRJDB12674 | ENA

The splicing activator DAZAP1 integrates splicing control into MEK/Erk regulated cell proliferation and migration

Project description:DAZAP1 was depleted in culterd HEK 293T cells using shRNA and the resulting poly A RNA were isolated c-DNA library constructed and paired end sequenced on illumina Hi-seq 2000 platform the data was compared to a control shRNA depleted cell

2013-12-25 | GSE52745 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data