Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

ABSTRACT: Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

PROVIDER: PRJNA1302476 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

Project description:The microarrays experiments was performed in order to identify transcriptional networks in Enterococcus faecalis. Work:Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure

2025-08-08 | GSE304768 | GEO

Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

Project description:Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

| PRJNA1150612 | ENA

Reduced glutathione levels in Enterococcus faecalis trigger metabolic and transcriptional compensatory adjustments during iron exposure.

Project description:Enterococcus faecalis, a facultative anaerobic pathogen and common constituent of the gastrointestinal microbiota, must navigate varying iron levels within the host. This study investigates the bacterium's response to elevated iron levels in the context of glutathione deficiency, a critical low molecular weight antioxidant synthesized within cells. We examined the transcriptomic and metabolic responses of a glutathione synthetase mutant strain (Δgsh) under conditions of increased iron, integrating these data into a genome-scale metabolic model (GSMM). Our findings reveal that, under glutathione deficiency, E. faecalis markedly reduces intracellular iron levels compared to the wild-type strain, with a reconfiguration of its global transcriptional response to prioritize the expression of genes involved in energy production. This transcriptional shift is associated with alterations in basal metabolites, notably an increase in arginine levels. The GSMM analysis underscores the significance of arginine metabolism as a potential compensatory mechanism for the diminished glutathione content during iron exposure, particularly highlighting the role of the arc operon (anaerobic arginine catabolism) in energy generation. This work provides crucial insights into the compensatory mechanisms related to metal homeostasis and the transcriptional and metabolic processes that mitigate the effects of reduced glutathione levels under oxidative stress induced by iron.

2026-09-17 | GSE275402 | GEO

Reduced glutathione levels in <i>Enterococcus faecalis</i> trigger metabolic and transcriptional compensatory adjustments during iron exposure.

Project description: Not available

| S-EPMC12817896 | biostudies-literature

Expression data of glutathione-fed Arabidopsis thaliana

Project description:To comprehensively investigate the effects of glutathione on the gene expression, the microarray analysis was performed in the glutathione-fed wild-type Arabidopsis thaliana. Wild-type Arabidopsis (ecotype Columbia-0) were fed with 1 mM oxidized glutathione (GSSG) and 2 mM reduced glutathione (GSH) for comparison at equal nitrogen equivalents. To examine the effects of glutathione other than nitrogen at equal nitrogen equivalents, plants were fed with 3 mM NH4NO3. Plants grown by water were used as a control.

2023-08-01 | GSE228403 | GEO

Interactions between H2O2 and glutathione in gene expression

Project description:rs08-03_glutathion - glutathion - How does glutathione content or reduction state affect H2O2-induced changes in the transcriptome? - Three single Arabidopsis mutants were used: cat2, knockout for catalase2 and so enriched in H2O2; cad2, defective in glutathione content; cytGR, knockout for cytosolic glutathione reductase. Cat2 was crossed with cad2 and cyt GR, and col0, 3 single mutants, and 2 double mutants were sampled in controlled growth conditions either in 8h or 16h photoperiod. Keywords: gene knock out 20 dye-swap pairs - CATMA arrays: 40 arrays

2010-07-22 | E-GEOD-21424 | biostudies-arrayexpress

glutathione s-transferase

Project description:production of glutathione s-transferase from Lactobacillus plantarum Ku720558

| PRJEB33504 | ENA

Tamarixetin induces ferroptotic stress through the SLC7A11–GPX4 axis and triggers a compensatory NRF2 response

Project description:Ferroptosis has emerged as a therapeutic vulnerability in hepatocellular carcinoma, but its interplay with antioxidant defense remains incompletely understood. Here, we investigated whether Tamarixetin induces ferroptotic stress in hepatoma cells and how nuclear factor erythroid 2-related factor 2 (NRF2) signaling responds to this process. Tamarixetin selectively reduced hepatoma cell viability, increased lipid peroxidation, and these effects were partially rescued by ferrostatin-1. Transcriptome analysis revealed enrichment of ferroptosis- and glutathione metabolism-related pathways, highlighting redox-associated genes centered on the SLC7A11–glutathione peroxidase 4 (GPX4) axis. Tamarixetin also increased NRF2 target gene expression, indicating activation of a compensatory antioxidant response to oxidative stress. Molecular docking further suggested a potential interaction between Tamarixetin and the xCT transporter. These findings identify Tamarixetin as a modulator of ferroptotic stress in hepatoma cells and support redox-targeting strategies for liver cancer.

2026-05-11 | GSE327198 | GEO

Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis

Project description:Organelle transporters define metabolic compartmentalization and how this metabolite transport process can be modulated is poorly explored. Here, we discovered that SLC25A39, a mitochondrial transporter critical for mitochondrial glutathione uptake, is a short-lived protein under dual regulation at the protein level. Co-immunoprecipitation mass spectrometry and CRISPR KO in cells identified that mitochondrial m-AAA protease AFG3L2 is responsible for degrading SLC25A39 through the matrix loop 1. SLC25A39 senses mitochondrial iron-sulfur cluster using four matrix cysteine residues and inhibits its degradation. SLC25A39 protein regulation is robust in developing and mature neurons. This dual transporter regulation, by protein quality control and metabolic sensing, allows modulating mitochondrial glutathione level in response to iron homeostasis, opening new avenues to explore regulation of metabolic compartmentalization. Neuronal SLC25A39 regulation connects mitochondrial protein quality control, glutathione and iron homeostasis, which were previously unrelated biochemical features in neurodegeneration.

2025-03-19 | PXD047327 | Pride

Expression data for plant compensatory responses

Project description:Plant compensatory responses depends on transcriptional reprogramming. We used microarray analysis to understand the differential gene expression pattern between clipped (herbivore browsed) and unclipped plant. Arabidopsis ecotypes Columbia and Landsberg erecta were chosen due to their differential compensatory response. The plants were grown in greenhouse. At bolting stage the plants were clipped to imitate herbivore damage. Following day the samples were collected from clipped and unclipped plants.

2013-03-02 | E-GEOD-44781 | biostudies-arrayexpress

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