Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of hPNPase on Escherichia coli transcritome after addition of rifampicin

ABSTRACT: We replaced the natural pnp locus with the human cDNA and studied the transcriptomes of 3 strains, namely the wt pnp+ (C-1a), the mutant with pnp ORF deletion (C-5691) and the strain with the substitution of the bacterial ORF with the human one (C-6001), before and 4 minutes after the addition of rifampicin to inhibit transcription.

ORGANISM(S): Escherichia coli

PROVIDER: GSE221825 | GEO | 2023/08/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of hPNPase on Escherichia coli transcritome

Project description:We replaced the natural pnp locus with the human cDNA and studied the transcriptomes of 3 strains, namely the wt pnp+ (C-1a), the mutant with pnp ORF deletion (C-5691) and the strain with the substitution of the bacterial ORF with the human one (C-6001).

2023-08-08 | GSE211960 | GEO

Transcription profiling by array of Rifampicin-induced transcriptome response in rifampicin-resistant Mycobacterium tuberculosis

Project description:Tuberculosis (TB) is still a major life-threatening infectious disease, within which especially the rise of multidrug resistant TB (MDR-TB) is currently worrying. This study focuses on mechanisms of development of rifampicin resistance, since rifampicin seems to play an important role in the development of MDR-TB. To provide further insight in rifampicin resistance, we performed a genome-wide transcriptional profile analysis for Mycobacterium tuberculosis (M. tuberculosis) using microarray technology and qRT-PCR analysis. We exposed a rifampicin-susceptible H37Rv wild type (H37Rv-WT) and a rifampicin-resistant progeny H37Rv strain with a H526Y mutation in the rpoB gene (H37Rv-H526Y) to several concentrations of rifampicin, to define the effect of rifampicin on the transcription profile. Our study showed that there are resistance-dependant differences in response between both M. tuberculosis strains. Gene clusters associated with efflux, transport and virulence were altered in the rifampicin-resistant H37Rv mutant compared to the rifampicin-susceptible H37Rv-WT strain after exposure to rifampicin. We conclude that the small gene cluster Rv0559c-Rv0560c in the H37Rv-H526Y strain was remarkably up-regulated in the microarray analysis and qRT-PCR results and appeared to be dependent on rifampicin concentration and time of exposure. Therefore this study suggests that Rv0559c and Rv0560c play a pivotal role in rifampicin resistance of M. tuberculosis. Further investigation of Rv0559c and Rv0560c is needed to reveal function and mechanism of both genes that were triggered upon rifampicin exposure. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-139]

2013-04-21 | E-BUGS-139 | biostudies-arrayexpress

Rifampicin-mouse liver proteomics

Project description:Tuberculosis is one of top causes of death among curable infectious diseases; it is an airborne infectious disease that kills 2 million people worldwide. Anti-tuberculosis drug-induced liver injury is the primary cause of drug-induced liver injury (DILI). Rifampicin is one of the most common anti-tuberculosis therapies and has well-known hepatotoxicity. To understand the mechanism of rifampicin-induced liver injury, we performed a global proteomic analysis of liver proteins by LC-MS/MS in a mouse model after the oral administration of 177 and 442.5 mg/kg rifampicin (LD10 and LD25) for 14 days. Based on the biochemical parameters in the plasma after rifampicin treatment, the hepatotoxic effect of rifampicin in the mouse liver was defined as a mixed liver injury. In the present study, we identified 1,101 proteins and quantified 1,038 proteins. A total of 29 and 40 proteins were up-regulated and 27 and 118 proteins were down-regulated in response to 177 and 442.5 mg/kg rifampicin, respectively.

2017-07-10 | PXD006313 | Pride

Caulobacter crescentus mRNA half-lives by rifampicin transcription shutoff

Project description:mRNA half-life profiling in the bacterium Caulobacter crescentus was preformed by shutting of transcription with the antibiotic rifampicin, and following mRNA abundance at 1, 2, 4, 8, and 15 minutes post rifampicin. All RNA measurements were performed on cells grown to mid-log in M2G minimal growth medium. Two biological replicates time coursees were collected from independent starter cultures.

2020-09-04 | GSE157432 | GEO

In vivo gene expression analysis of C elegans in response to rifampicin

Project description:We have discovered rifampicin as a glycation inhibitor, which increases life span in C elegans. In order to understand the mechanism of rifampicin action, microarray analysis was performed to study the changes in gene expression brought about by the drug.

2014-12-31 | GSE45292 | GEO

Rifampicin test as a predictor of Irinotecan toxicity in metastatic colorectal cancer.

Project description:Interventions: The patients with metastatic colorectal cancer being considered for Irinotecan treatment will take single 900 mg dose of oral rifampicin. Bilirubin levels will be measured after 4 hours. The patients will go on to have standard Irinotecan treatment. There will be at least 48 hours interval between rifampicin ingestion and irinotecan treatment. They will be monitored for toxicities especially diarrhoea and neutropenia after cycle 1 irinotecan. A correlation will be done between rise in bilirubin and toxicities. Both the intervention- rifampicin intake and irinotecan administration will be on a single day only 2 days apart. Patients will be monitored for 3 weeks after irinotecan dose for toxicities. Blood will also be analysed for UGT 1A1 polymorphism and correlated with toxicities and rise in bilirubin. Primary outcome(s): To determine if rifampicin induced hyperbilirubinemia can predict irinotecan toxicity.[Measured on day 21 after irinotecan dose.] Study Design: Purpose: Diagnosis; Allocation: Non-randomised trial; Masking: Open (masking not used);Assignment: Single group;Type of endpoint: Safety

| 2453055 | ecrin-mdr-crc

Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome

Project description:This SuperSeries is composed of the following subset Series: GSE24186: Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome [Steroltalk platform] GSE24187: Atorvastatin, rosuvastatin and rifampicin effect on human primary hepatocyte transcriptome [Affymetrix platform] Refer to individual Series

2011-09-04 | E-GEOD-24188 | biostudies-arrayexpress

The effect of rifampicin on human mononuclear cell gene expression

Project description:The aim of the study was to elucidate the effects of pregnane receptor X (PXR) activation by rifampicin on the mononuclear cell gene expression in vivo.

2020-03-23 | GSE108100 | GEO

Measuring gene expression in serially-evolved E. coli BW25113 strains in M9+glucose and M9+glucose+rifampicin

Project description:We measured steady-state E. coli transcript levels in 1) a pykF(C8Y) mutant, 2) a rpoB(T1037P) mutant, and 3) five rifampicin-resistant rpoB mutant strains selected from each of these single mutants, in the presence and absence of rifampicin.

2020-10-23 | GSE136977 | GEO

Transcriptome Profiling for Escherichia coli K12 wild type and ΔcsdA mutant before and after rifampicin-treatment

Project description:The cell cycle coordinates with growth to ensure suitable genome inheritance. The CsdA protein is a highly conserved, DEAD-box RNA helicase and assists RNA structural remodeling at low temperature. The absence of CsdA yields a severe growth defect manifested by increased doubling time, more extensive cell size, or slower colony growth at low temperature. Nevertheless, it is unknown how the lack of CsdA at low temperature affects the cell cycle and the causes of the yield of severe growth defect phenotypes. This work shows that the lack of CsdA results in incoordination of the cell cycle to growth at low temperature. We performed microarray analyses to compare the transcriptome profiles of ΔcsdA mutant with WT cell before and after rifampicin-treatment in LB to understand how the lack of CsdA at low temperature affects the cell cycle and the causes of the yield of severe growth defect phenotypes.

2023-12-30 | GSE206007 | 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