Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

WT and lincRNA-EPS knockout iBMMs that infected with VSV or not

ABSTRACT: WT and lincRNA-EPS knockout iBMMs that infected with VSV or not

PROVIDER: PRJNA795791 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17514833_1.fastq.gz	Fastqsanger.gz
	SRR17514833_2.fastq.gz	Fastqsanger.gz
	SRR17514834_1.fastq.gz	Fastqsanger.gz
	SRR17514834_2.fastq.gz	Fastqsanger.gz
	SRR17514835_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

WT and lincRNA-EPS knockout iBMMs that infected with VSV or not

Project description:Test transcripts in mock and VSV infected WT and lincRNA-EPS knockout iBMMs

2022-01-12 | GSE193324 | GEO

WT and lincRNA-EPS knockout iBMMs that knocked down PKR or not

Project description:Test transcripts in control and siPKR WT and lincRNA-EPS knockout iBMMs

2022-01-12 | GSE193325 | GEO

A long noncoding RNA lincRNA-EPS acts as a transcriptional brake to restrain inflammation

Project description:LincRNA-EPS is a long noncoding RNA that is expressed in macrophages and downregulated upon exposure to diverse microbial products. Analysis of macrophages from lincRNA-EPS-deficient mice revealed a specific role for this lincRNA in restraining immune response gene (IRG) expression. Mechanistically, lincRNA-EPS associates with chromatin at regulatory regions of IRGs to repress their transcription. To gain insight into the molecular function of lincRNA-EPS on chromatin, we generated ATAC-Seq libraries from wildtype and lincRNA-EPS-deficient macrophages stimulated with LPS.

2016-05-08 | GSE78873 | GEO

WT and lincRNA-EPS knockout iBMMs that knocked down PKR or not

Project description:WT and lincRNA-EPS knockout iBMMs that knocked down PKR or not

| PRJNA795804 | ENA

A long noncoding RNA lincRNA-EPS acts as a transcriptional brake to restrain inflammation

Project description:RNA-seq was performed in biological replicates (2 mice per group) of wild-type and lincRNA-EPS-/- BMDMs at 0, 2, and 6 hours after LPS treatment (100 ng/ml). RNA-seq libraries were prepared as described (Heyer et al., 2015). Briefly, ribosomal RNA (rRNA) was depleted using the Ribozero rRNA removal kit (Epicentre). Purified mRNAs were fragmented with RNA fragmentation reagent (Life Technologies) for 4 minutes and 30 seconds at 70C to obtain 100-150 nt long RNA fragments. After ethanol precipitation and washing, RNAs were re-suspended in 5 l of water and the 3 ends dephosphorylated using PNK (New England BioLabs) for 1 hr at 37C. RNA fragments with a 3 OH were then ligated to a preadenylated DNA adaptor using T4 RNA ligase 2, truncated K227Q (NEB). Following this, ligated RNAs were reverse-transcribed with Superscript III (Invitrogen) using a bar-coded reverse-transcription primer that anneals to the preadenylated adaptor. After reverse-transcription, gel purified cDNAs were circularized using CircLigase I (Epicentre) and PCR amplified using paired-end primers PE1.0 and PE2.0 (Illumina) for 14 cycles. PCR amplicons were gel purified and submitted for sequencing on the Illumina Hiseq2000. Tophat version 2.0.12 was used to align single sequence reads to version 73 of the Ensembl mouse genome (mm10) with options: --library-type fr-firststrand -g 1 -x 1 --read-mismatches 2. Cufflinks version 2.1.1 was used to estimate RNA abundances with Ensembl version 73 GTF and the --library-type fr-firststrand option. The Cuffdiff program was used to perform differential expression analysis between wild-type BMDMs and lincRNA-EPS-/- BMDMs at each corresponding time (0,2, and 6 hours after LPS treatment). To compute fold-change values for genes/transcripts with FPKM values of zero, a pseudocount of 1 was added to all FPKM values first.

2016-07-29 | E-MTAB-4088 | biostudies-arrayexpress

Wild-type and GLO2 knockout BMDMs with infection of VSV

Project description:Transcriptome analysis of wild-type and GLO2 knockout BMDM infected with VSV for 12 hours .

2024-07-01 | GSE248885 | GEO

RNA-Seq characterization of select lincRNA knockout mouse models

Project description:It has become clear that long intergenic noncoding RNAs (lincRNAs) are an important layer of genome regulation. Thousands have been identified in mammals, yet only a few have been tested through genetic ablation in animal models. Of the few that have, many yields weak to unobservable phenotypes, raising the question of their in vivo relevance. To more broadly investigate the functional relevance of lincRNAs in physiological conditions, we developed a collection of 18 lincRNA knockout strains. We found that two knockout strains, linc-Sox2 and linc-Foxf1a (Fendrr), exhibit perinatal lethal phenotypes in addition to multiple developmental abnormalities. Notably, in depth analysis of a third mutant strain, linc-Brn1b-/-, revealed defects in brain development, with distinct abnormalities in class-specific generation of upper layer II/III-IV neurons in the neocortex. Thus far, we found at least 6 of 18 mutant strains exhibit distinct developmental or lethality phenotypes. Therefore, this study demonstrates that lincRNAs are required for life and play critical roles during mammalian development, highlighting the importance of studying them further to better understand the molecular mechanisms leading to disease. Minimum 2 replicates each of select wild type and lincRNA knockout embryonic and postnatal tissues for three distinct lincRNA knockout mouse strains.

2013-11-30 | E-GEOD-49581 | biostudies-arrayexpress

Effect of lincRNA-p21 knockout (KO) in ventricles 8 weeks after sham/Transverse aortic restriction (TAC) surgeries

Project description:Cardiac hypertrophy is an adaptive response to pressure overload aimed at maintaining cardiac function. However, prolonged hypertrophy significantly increases the risk of maladaptive cardiac remodeling and heart failure. The role of cardiac long non-coding RNAs in cardiac hypertrophy and cardiomyopathy is not well understood. lincRNA-p21 was induced in mouse and human cardiomyopathy tissue. Global and cardiac-specific lincRNA-p21 knockout significantly suppressed pressure overload-induced ventricular wall thickening, stress marker elevation, and deterioration of cardiac function. Genome-wide transcriptome analysis and transcriptional network analysis revealed that lincRNA-p21 acts in trans to stimulate the NFAT/MEF2 pathway. Mechanistically, lincRNA-p21 bound to the scaffold protein KAP1. lincRNA-p21 cardiac-specific knockout suppressed stress-induced nuclear accumulation of KAP1, and KAP1 knockdown attenuated cardiac hypertrophy and NFAT activation. KAP1 positively regulated pathological hypertrophy by physically interacting with NFATC4 to promote the overactive status of NFAT/MEF2 signaling. Importantly, GapmeR ASO depletion of lincRNA-p21 similarly inhibited cardiac hypertrophy and adverse remodeling, highlighting the therapeutic potential of inhibiting lincRNA-p21.

2024-06-11 | GSE262894 | GEO

A long noncoding RNA lincRNA-EPS acts as a transcriptional brake to restrain inflammation

Project description:A long noncoding RNA lincRNA-EPS acts as a transcriptional brake to restrain inflammation

| PRJEB11889 | ENA

LincRNA-EPS negatively regulates host antiviral immunity by antagonizing viral RNA interacting with PKR

Project description:LincRNA-EPS negatively regulates host antiviral immunity by antagonizing viral RNA interacting with PKR

| PRJNA795796 | ENA