Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Heart RNA-seq of control mice and mice with titin PEVK domain knockout, Rbm20 RNA recognition motif knockout, or double knockout

ABSTRACT: We report the heart RNA-sequencing of control animals (129S6 genetic background, wild type). Animal models comprise of Titin PEVK homozygous deletion of exons 219-225 (PEVK-KO), RBM20 heterozygous deletion of exons 6-7 (RBM20-HET), and double deletion (PEVK-KOxRBM20-HET). RNA from left ventricular tissue was isolated using TRIzol followed by a clean-up with the QIAGEN RNA micro kit, cDNA libraries were generated using the Illumina TruSeq Stranded mRNA Sample Prep Kit 2x101 paired-end sequenced on HiSeq2000 (WT, RBM20-HET) or HiSeq4000 (PEVK-KOxRBM20-HET). Trimming and quality clipping was performed with Flexbar v. 3.03. The remaining reads greater than 18bp were mapped to the murine genome (assembly EnsEMBL 84) with the splice-aware STAR aligner v. 2.5.1b. Transcriptome analyses on differential gene and isoform abundance were carried out with cuffdiff 20 v. 2.2.1.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Mus musculus

SUBMITTER:

PROVIDER: E-MTAB-11124 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP132990

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

TMT isobaric profiling of PPIA heterozygous versus knockout haematopoietic stem cells

Project description:Mass spectrometry was performed with an Orbitrap Fusion Tribrid mass spectrometer (Thermo Scientific) interfaced with an UltiMate 3000 Binary RSLCnano System (Dionex). Proteome Discoverer v.1.4 (Thermo Scientific) with SEQUEST HT search engines was used for the spectra-preprocessing and HCD MS2 spectra were used for peptide identification and quantitation based on TMT reporter ions. TMT isobaric comparison of Ppia heterozygous (het) versus knockout (KO) haematopoietic stem and progenitor cells. Het 1 is sample 126 and KO 1 is sample 131 of dataset UTH_2. Het 2 and KO 2 are samples 126 and 127 of UTH_4. Het 3 and KO 3 are samples 130 and 127 of dataset UTH_3.

2023-10-16 | MSV000093127 | MassIVE

Lung-resident myeloid-derived suppressor cells display dual functionality in experimental tuberculosis

Project description:Using cell-based approaches and experimental mouse models for pulmonary TB we unveiled MDSCs as new myeloid populations directly interacting with Mycobacterium tuberculosis (Mtb). MDSCs readily phagocytosed Mtb, released proinflammatory (IL-6, IL-1M-NM-1) and immunomodulatory (IL-10) cytokines while retaining their suppressive capacity. MDSCs were identified at the site of infection in disease-resistant and -susceptible mice during pulmonary TB. Excessive MDSC accumulation in lungs correlated with elevated surface expression of IL-4RM-NM-1 and heightened TB lethality. Microarray experiments were performed as dual-color hybridizations on Agilent mouse whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.

2014-12-21 | E-GEOD-57124 | biostudies-arrayexpress

Aberrant developmental titin splicing and dysregulated sarcomere length in Thymosin β4 knockout mice.

Project description:Sarcomere assembly is a highly orchestrated and dynamic process which adapts, during perinatal development, to accommodate growth of the heart. Sarcomeric components, including titin, undergo an isoform transition to adjust ventricular filling. Many sarcomeric genes have been implicated in congenital cardiomyopathies, such that understanding developmental sarcomere transitions will inform the aetiology and treatment. We sought to determine whether Thymosin β4 (Tβ4), a peptide that regulates the availability of actin monomers for polymerization in non-muscle cells, plays a role in sarcomere assembly during cardiac morphogenesis and influences adult cardiac function. In Tβ4 null mice, immunofluorescence-based sarcomere analyses revealed shortened thin filament, sarcomere and titin spring length in cardiomyocytes, associated with precocious up-regulation of the short titin isoforms during the postnatal splicing transition. By magnetic resonance imaging, this manifested as diminished stroke volume and limited contractile reserve in adult mice. Extrapolating to an in vitro cardiomyocyte model, the altered postnatal splicing was corrected with addition of synthetic Tβ4, whereby normal sarcomere length was restored. Our data suggest that Tβ4 is required for setting correct sarcomere length and for appropriate splicing of titin, not only in the heart but also in skeletal muscle. Distinguishing between thin filament extension and titin splicing as the primary defect is challenging, as these events are intimately linked. The regulation of titin splicing is a previously unrecognised role of Tβ4 and gives preliminary insight into a mechanism by which titin isoforms may be manipulated to correct cardiac dysfunction.

| S-EPMC5319848 | biostudies-literature

Telomeric retrotransposon HeT-A contains a bidirectional promoter that initiates divergent transcription of piRNA precursors in Drosophila germline

Project description:PIWI-interacting (pi) RNAs provide silencing of transposable elements (TE) in the germline. Drosophila telomeres are maintained by transpositions of specialized telomeric retroelements. piRNAs generated from sense and antisense transcripts of telomeric elements provide telomere length control in the germline. Previously, we have found that antisense transcription of the major telomeric retroelement HeT-A is initiated upstream of the HeT-A sense transcription start site. Here, we performed a deletion analysis of the HeT-A promoter and show that common regulatory elements are shared by sense and antisense promoters of HeT-A. Therefore, the HeT-A promoter is a bidirectional promoter capable of processive sense and antisense transcription. Ovarian small RNA data shows that a solo HeT-A promoter within an euchromatic transgene initiates divergent transcription of transgenic reporter genes and subsequent processing of these transcripts into piRNAs. These events lead to the formation of a divergent uni-strand piRNA cluster at solo HeT-A promoters, in contrast to endogenous telomeres that represent strong dual-strand piRNA clusters. Solo HeT-A promoters are not immunoprecipitated with Heterochromatin Protein 1 (HP1) homolog Rhino, a marker of the dual-strand piRNA clusters, but are associated with HP1 itself, which provides piRNA-mediated transcriptional repression of the reporter genes. Unlike endogenous dual-strand piRNA clusters, the solo HeT-A promoter does not produce overlapping transcripts. In a telomeric context, however, bidirectional promoters of tandem HeT-A repeats provide read-through transcription of both genomic strands, followed by Rhi binding. These data indicate that Drosophila telomeres share properties of uni-strand and dual-strand piRNA clusters.

2016-12-07 | GSE78135 | GEO

A senescence-inflammatory switch from cancer-inhibitory to cancer-promoting mechanism

Project description:To elucidate the effect of senescence in mouse colorectal tumor, the transcriptome of enterocytes from CKI alpha deletion mutants (CKI alpha KO), CKI alpha/p53 double deletion mutants (CKI alpha/p53 DKO) and CKI alpha heterozygous mice (CKI alpha Het) were determined by RNAseq.

2013-06-12 | E-MTAB-1683 | biostudies-arrayexpress

Cullin 3 Mouse Brain TMT-based Proteomics Analysis

Project description:This project consists in 3 datasets: - Samples from adult mouse brains (Hippocampus, Cortex and Cerebellum): Cul3 +/- or +/+; 5 animals per condition. - Samples from embryonic mouse cortex: either Cul3 +/- or +/+ - Samples from embryonic mouse cortex: Cul3 fl/fl Emx-1-Cre ("hom"); Cul3 +/fl Emx1-Cre ("het") or Cul3+/fl ("control")

2021-03-26 | PXD017040 | Pride

Reduced Slc1a1 expression is associated with neuroinflammation and impaired sensorimotor gating and cognitive performance in mice: implications for schizophrenia

Project description:We characterized the in vivo and in vitro consequences of reduced expression of Slc1a1 in mice. Heterozygous (HET) Slc1a1+/- mice, which model the hemi-deletion we found in human subjects with schizophrenia, were examined in a series of behavioral, anatomical and biochemical assays. Knockout (KO) mice were also included in the behavioral studies for comparative purposes. Both HET and KO mice exhibited evidence of increased anxiety-like behavior, impaired working memory, decreased exploratory activity and impaired sensorimotor gating, but no changes in overall locomotor activity compared to wildtype (WT) mice. The magnitude of changes was approximately equivalent in the HET and KO mice suggesting a dominant effect of the haploinsufficiency. Whole transcriptome RNA-Seq analysis detected expression changes of genes and pathways involved in cytokine signaling and synaptic functions in both brain and blood of the HET mice compared to WT mice.

2017-08-29 | GSE103194 | GEO

Next Generation Sequencing Analysis of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

Project description:mRNA profiles of chemically reprogrammed osteoblasts from Beta-actin Wildtype (WT) Heterozygotes (HET) and knockout (KO) Mouse Embryonic Fibroblast (MEFs)

2019-08-06 | GSE135392 | GEO

Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia

Project description:Distinct genetic abnormalities such as TP53 deletion at 17p13.1, have been identified as having an adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL). Conventional cytogenetic studies have shown that TP53 deletion in B-CLL is associated predominantly with 17p loss resulting from complex chromosomal rearrangements. We performed genome-wide DNA (SNPs arrays), fluorescence in situ hybridization (FISH) and gene expression profiling (GEP) analyses to investigate the significance of 17p loss in a panel of 71 genetically well-characterized B-CLLs in Binet stage A, 18 of which carried a TP53 monoallelic deletion. Combined SNP arrays and FISH approaches showed 17p loss in all of the TP53-deleted cases, with breakpoints scattered along the 17p11.2 region. Mutations in exons 5 to 9 of TP53 were found in 9/12 deleted samples. GEP of 60 B-CLLs, including 7 patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were down-regulated in 17p- tumors. The majority (30/35) of these transcripts, including putative tumor suppressor genes, mapped to 17p. Overall, these data indicate that, beside TP53 deletion, the concomitant loss of 17p arm may contribute to the strong negative prognostic impact known to be associated with this lesion in B-CLL. This SuperSeries is composed of the following subset Series: GSE9992: Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment A GSE11036: Molecular and transcriptional characterization of chromosome 17p loss in chronic lymphocytic leukemia, experiment B Keywords: SuperSeries Refer to individual Series

2008-11-11 | E-GEOD-11038 | biostudies-arrayexpress

Predictive value of drug elimination gene polymorphisms on clearance and dose adjustment of sunitinib (Sutent, SU11248) in patients with cancer

Project description:Primary objectives: To observe the correlation between ABCB1 polymorphisms in Exons 13, 22 and 27 and the clearance of sunitinib at steady state. Primary endpoints: The endpoint of the study is a correlation between sunitinib clearance and toxicityadjusteddose with ABCB1 genotype examining SNPs in exons 13, 22,and 27 as wellas haplotypes of these exons.

| 2525144 | ecrin-mdr-crc

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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