Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NS-NHE-2016-S-1

ABSTRACT: NS-NHE-2016-S-1 Metagenome

PROVIDER: PRJNA656712 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12550375_1.fastq.gz	Fastqsanger.gz
	SRR12550375_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

NS-NHE-PGPR-2016-S2

Project description:NS-NHE-PGPR-2016-S2 Metagenome

| PRJNA656688 | ENA

NS-NHE-PHE-2016-C

Project description:NS-NHE-PHE-2016-C Metagenome

| PRJNA656705 | ENA

NS-PHE-2016-S4

Project description:NS-PHE-2016-S4 Metagenome

| PRJNA656711 | ENA

NS-PHE-PGPR-2016-S3

Project description:NS-PHE-PGPR-2016-S3 Metagenome

| PRJNA656696 | ENA

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

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

Differential gene expression in mACVR1 NS v wt-ACVR1 NS.

Project description:To study the effect of the ACVR1 G328V mutation in tumor neurospheres with a background of NRASV12 overexpression and p53 knockdown. The goal of this study was to identify differentially expressed genes between mACVR1 NS v wt-ACVR1 NS.

2020-04-16 | GSE148732 | GEO

Analysis of Wild Type, H-NS KO and cover mutated H-NS Transcriptomes

Project description:The goals of this study are to compare the difference transcriptome of Wild Type, H-NS KO and cover mutated H-NS by RNA-seq

2021-03-25 | GSE169499 | GEO

NS-PAH-2015-PNP-5

Project description:NS-PAH-2015-PNP-5 Metagenome

| PRJNA587569 | ENA

Esophageal Squamous Cell Carcinoma tumors from Indian patients: nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein

Project description:Transcriptional profiling of Esophageal Squamous Cell Carcinoma (ESCC) tumors comparing samples harbouring nuclear-stabilized p53 (NS+) versus unstable p53 (NS-) protein, determined through immunohistochemistry (IHC) staining of the tumor sections. The goal was to identify the genes that were differentially regulated between NS+ and NS- ESCC samples.

2024-03-29 | GSE218109 | 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