Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NS-PAH-2015-PNP-5

ABSTRACT: NS-PAH-2015-PNP-5 Metagenome

PROVIDER: PRJNA587569 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10426077_1.fastq.gz	Fastqsanger.gz
	SRR10426077_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Polyaromatic hydrocarbon metagenome

Project description:Metagenome diversity in polyaromatic hydrocarbon (PAH) degrading consortium (NS-PAH-2015-HSR-4)

| PRJNA587568 | ENA

Transcriptomic Analysis of pnp-1 mutants in C. elegans

Project description:We used RNA-seq to identify gene expression changes in C. elegans pnp-1 mutants

2021-04-14 | GSE165786 | GEO

Pseudomonas sp. PNP

Project description:Pseudomonas sp. PNP Genome sequencing and assembly

| PRJNA717186 | ENA

Comprehensive transcriptome analysis of the heart in control, PAH and PAH/aKO mice.

Project description:Pregnancy-associated hypertensive (PAH) mice were maintained by mating females carrying the human angiotensinogen (hAGT) gene with males expressing the human renin (hRN) gene, as previously described (Takimoto E., et al., Science, 1996). Angiotensin II (AngII) has critical roles in regulation of blood pressure. In late pregnancy of PAH mice, increased AngII causes acute and severe hypertension with proteinuria. Furthermore, PAH mice show cardiac hypertrophy, fibrosis and apoptosis. It is known that AngII downregulates mRNA of alpha 1a-adrenergic receptor (Adra1a) in neonatal rat cardiac myocytes (Li H.T., et al., Circ. Res., 1997). Interestingly, we found that Adra1a knock out PAH (PAH/aKO) mice display more severe phenotype of cardiac hypertrophy in comparison to PAH mice. In this study, to understand the molecular basis of cardiac hypertrophy via regulation of Adra1a expression with AngII in PAH mice, we performed a comprehensive analysis of gene expression changes in cardiac remodeling of PAH and PAH/aKO mice using the next-generation RNA sequencing (RNA-seq).

2023-01-27 | GSE140948 | GEO

Reversible and irreversible PAH in a rat model for MCT+Shunt-induced PAH and hemodynamic unloading.

Project description:PAH was induced by 60mg/kg MCT and an aorto-caval shunt. At different timepoints of PAH progression (day 14, 21 and 28 after MCT-injection), the left lung with PAH was hemodynamically unloading by unilateral orthotopic transplatation into a syngeneic, healthy recipient. All day 14 and 7/10 day 21 transplanted lungs showed reversal of PAH after LTx. All day 28 and 3/10 day 21 transplanted lungs showed PAH progression after LTx. Lung tissue of Reversible and Irreversible PAH and normal controls, acquired at LTx, was compared using RNA-seq.

2020-07-01 | GSE149899 | GEO

NS-PHE-2016-S4

Project description:NS-PHE-2016-S4 Metagenome

| PRJNA656711 | ENA

Transcription profiling by array of Staphylococcus aureus wild type and rnc, pnp and sigB mutants

Project description:Transcriptome mapping of Staphylococcus aureus wild type and rnc, pnp and sigB mutants

2010-12-31 | E-MEXP-2778 | biostudies-arrayexpress

Oral tongue cancer: p53 NS+ vs. p53 NS- tumor

Project description:Transcriptional profiling of squamous cell carcinoma of oral tongue, comparing p53 NS+ and p53 NS- tumors. Goal was to determine differentially expressed genes between them based on global gene expression.

2020-05-04 | GSE89146 | GEO

PNP mediated guanosine induced gene expression

Project description:PNP mediated guanosine induced gene expression

| PRJNA910499 | ENA

RfaH counter-silences inhibition of transcript elongation by H-NS–StpA H-NS nucleoprotein filaments in pathogenic E. coli

Project description:Expression of virulence genes in pathogenic E. coli is controlled in part by the transcription silencer H-NS and its paralogs (e.g., StpA), which sequester DNA in multi-kb nucleoprotein filaments to inhibit transcription initiation, elongation, or both. Some activators counter-silence initiation by displacing H-NS from promoters. How H-NS inhibition of elongation is overcome is not understood. In uropathogenic E. coli (UPEC), elongation regulator RfaH aids expression of some H-NS-silenced pathogenicity operons (e.g., hlyCABD encoding hemolysin). RfaH associates with elongation complexes (ECs) via direct contacts to a transiently exposed, nontemplate DNA-strand sequence called ops (operon polarity suppressor). RfaH–ops interactions establish long-lived RfaH–EC contacts that allow RfaH to recruit ribosomes to the nascent mRNA and to suppress transcriptional pausing and termination. Using ChIP-seq, we mapped the genome-scale distributions of RfaH, H-NS, StpA, RNA polymerase (RNAP), and σ70 in the UPEC strain CFT073. We identify 8 RfaH-activated operons, all of which were bound by H-NS and StpA. Four are new additions to the RfaH regulon. Deletion of RfaH caused premature termination whereas deletion of H-NS and StpA allowed elongation without RfaH. Thus, RfaH is an elongation counter-silencer of H-NS. Consistent with elongation counter-silencing, deletion of StpA alone decreased the effect of RfaH. StpA increases DNA bridging, which inhibits transcript elongation via topological constraints on RNAP. Residual RfaH effect when both H-NS and StpA were deleted was attributable to targeting of RfaH-regulated operons by a minor H-NS paralog, Hfp. These operons have evolved higher levels of H-NS–binding features, explaining minor-paralog targeting.

2022-10-06 | GSE212064 | GEO

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