Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enterohemorrhagic Escherichia coli O157:H7 responds to norepinephrine gradients by tRNA reprogramming and codon-biased translation of virulence genes

ABSTRACT: We grew Escherichia coli O157:H7 strain EDL933 in low glucose DMEM and exposed it to 0 and 50 micromolar norepinephrine. After 5 hr of growth (37C, shaking 180rpm), cells were pelleted. Protein was then extracted and prepared for TMT-tagged proteomics to analyze for differential protein expression.

INSTRUMENT(S):

ORGANISM(S): Escherichia Coli

SUBMITTER: Abigail McShane

LAB HEAD: Peter Dedon

PROVIDER: PXD068911 | Pride | 2026-04-17

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	FX1.raw	Raw
	FX1_2.raw	Raw
	FX1_3.raw	Raw
	FX2.raw	Raw
	FX2_2.raw	Raw

Items per page:

1 - 5 of 26

Similar Datasets

Transcription profiling of Dictyostelium discoides mutant cell type aspidocyte induced by heavy meatals and antibiotics

Project description:We describe the serendipitous discovery and first characterization of a new resistant cell type from Dictyostelium, which we propose to call the aspidocyte (aspida: Greek for shield). These cells are induced from amoebae by a range of toxins including heavy metals and antibiotics, and were first detected by their striking resistance to detergent lysis. Aspidocytes are separate, rounded or irregular shaped cells that are immotile but remain fully viable; once the toxic stress is removed, they revert to amoeboid cells within an hour. Induction takes a few hours and is completely blocked by the protein synthesis inhibitor cycloheximide. Aspidocytes lack a cell wall and their resistance to detergent lysis is active, requiring continued energy metabolism, and may be assisted by a complete cessation of endocytosis, as measured by uptake of the dye FM1-43. Microarray analysis shows that aspidocytes have a distinct pattern of gene expression with a number of genes up-regulated that are predicted to be involved in lipid metabolism. Aspidocytes were initially detected in a hypersensitive mutant, in which the AMP deaminase gene is disrupted, suggesting that the inductive pathway involves AMP levels or metabolism. Since aspidocytes can also be induced from wild-type cells and are much more resistant than amoebae to a membrane disrupting antibiotic, it is possible that they are an adaptation allowing Dictyostelium cells to survive a sudden onslaught of toxins in the wild.

2007-02-06 | E-SGRP-5 | biostudies-arrayexpress

Impact of Glucocorticoids and PI3K Inhibition on Gene Expression in Myeloma

Project description:We previously noted that combination glucocorticoids and PI3K inhibition induces synergistic cell death. To identify genes involved in myeloma cell death we examined mRNA expression in each individual treatment and in the combination. The glucocoriticoid resistant cells (MM.1RL) are used as a negative control. Gene expression is assessed using Illumina Human HT-12v4 bead chips For this experiment, the lab is using human multiple myeloma cell lines that were isolated from a patient. MM.1S cells display sensitivity to glucocorticoids. MM.1RL cells display resistance to glucocorticoid treatment due to spontaneous mutations that render the glucocorticoid receptor inoperable. In this experiment, there will be 4 conditions for the MM.1S cells, and 2 conditions for the MM.1RL cells. We will be treating the MM.1S cells with a glucocorticoid alone (Dexamethasone - 1 uM), a PI3K inhibitor alone (LY249002 - 25 uM), a combination of the two drugs, and a vehicle control. The MM.1RL cells will be treated with a PI3K inhibitor alone, and with a vehicle control. Since the PI3K inhibitor is diluted in DMSO, as a control an equal volume of DMSO will be added to all conditions not containing the PI3K inhibitor. Conditions within the MM.1S cell line will be compared with each other. Specifically, we hope to identify genes that are similarly affected by all three experimental conditions. The MM.1RL conditions will not be analyzed at this time. There will be 4 biological replicates of each condition.

2015-12-07 | E-GEOD-64704 | biostudies-arrayexpress

RNAseq of Human Umbilical Vein Endothelial Cells treated with Insulin in the presence or absence of TGF-beta kinase inhibitor SB431542 for 90 minute.

Project description:Endothelial cells play many important role during development and development of diseases. Endothelial dysfunction which is commonly seen in diabetes patients is thought to be one of the first step that leads to adverse events such as retinopathy, nephropathy, and atherosclerosis. To examine to which extent TGF-beta signaling contributes to insulin-induced transcriptional responses we performed this RNAseq on Human umbilical vein endothelial cells.

2019-01-15 | E-MTAB-6841 | biostudies-arrayexpress

Differential Chemoproteomics Reveals MARK2/3 as Cell Migration-Relevant Targets of the ALK Inhibitor Brigatinib

Project description:Metastasis poses a major challenge in cancer management, including EML4-ALK-rearranged non-small cell lung cancer (NSCLC). As cell migration is a critical step during metastasis, we assessed the anti-migratory activities of several clinical ALK inhibitors in NSCLC cells and observed differential anti-migratory capabilities despite similar ALK inhibition, with brigatinib displaying superior anti-migratory effects over other ALK inhibitors. Applying an unbiased in-situ mass spectrometry-based chemoproteomics approach, we determined the proteome-wide target profile of brigatinib in EML4-ALK+ NSCLC cells. Dose-dependent and cross-competitive chemoproteomics suggested MARK2 and MARK3 as relevant brigatinib kinase targets. Functional validation showed that combined pharmacological inhibition or genetic modulation of MARK2/3 inhibited cell migration. Consistently, brigatinib treatment induced inhibitory YAP1 phosphorylation downstream of MARK2/3. Collectively, our data suggest that brigatinib exhibits unusual cross-phenotype polypharmacology as despite similar efficacy for inhibiting EML4-ALK-dependent cell proliferation as other ALK inhibitors, it more effectively prevented migration of NSCLC cells due to co-targeting of MARK2/3.

2024-04-05 | PXD036716 | Pride

The Role of LVV-H7 in Alcohol-Induced Reward Mechanisms

Project description:Hemorphins are short peptides generated during cleavage of the hemoglobin chains but alpha chain, with various functions in different systems and tissues in both physiology and pathophysiology. The main purpose of this study was to establish the role of LVV-H7 in the mechanism of alcohol dependence. LVV-hemorphin 7 (LVV-H7) is released at higher concentrations in the presence of alcohol in vitro. Therefore, we predicted that alcohol intake can change the level of LVV-H7. We have accomplished behavioral tests in animal studies, along with proteomic analysis of the CNS tissues of alcohol addicted rats to verify the correlation of LVV-H7 level and ethanol dependence. We have also confirmed the BBB permeability of synthesized LVV-H7, as well as an inhibitor of its releasing enzyme- pepstatin using fluorescent microscopy. We have found a dose-dependent correlation between LVV-H7 and the time spent by rats in the drug-associated compartment using CPP test. Utilizing mass spectrometry-based methods we identified protein binding targets of LVV-H7 in the CNS tissue of addicted rats, along with the LVV-H7 degrading enzymes. The interpretation of the obtained results reveals the substantial role of LVV-H7 in the mechanism of alcohol dependence.

2025-09-05 | PXD036448 | Pride

Trivalent arsenic inhibits the functions of chaperonin complex

Project description:The goal of this study was to identify yeast mutants with arsenite hypersensitivity. Keywords: dose response Matched pools of yeast knockout (YKO) mutants were grown in paired growth media lacking or containing arsenite at various concentrations. The relative abundances of the YKO mutants were profiled using microarrays. Three types of pools were used in this study: (1) heterozygous diploid mutants; (2) haploid mutants obtained as progeny from the heterozygous diploid pool; and (3) haploid mutants also containing a null mutation of the prefoldin gene PFD1.

2010-07-26 | E-GEOD-5973 | biostudies-arrayexpress

A genome-wide CRISPR interference screen using an engineered trafficking biosensor reveals a role for DNAJC13 in opioid receptor downregulation

Project description:G protein-coupled receptor (GPCR) activity is critically regulated by trafficking through the endo-lysosomal pathway. Identifying the genes involved in GPCR trafficking is challenging due the complexity of sorting operations and low affinity protein-receptor interactions. Here we show that the engineered enzyme APEX2 is a highly sensitive biosensor for GPCR trafficking to the lysosome, and this trafficking can be monitored through APEX-based activation of fluorogenic substrates such as Amplex UltraRed (AUR). Using our GPCR-APEX2/AUR pipeline, we demonstrate that a gene identified in our screen, DNAJC13, plays a conserved role in the trafficking of activated DOR to the lysosome. To determine how depletion of DNAJC13 changes the local proteome of DOR-positive endosomes in cultured cells, we made cell lines stably expressing DOR-APEX2 or GFP-APEX2 (cytoplasmic). We then used siRNAs to knockdown DNAJC13 from DOR-APEX2 cells and compared these results to a siRNA control. Three independent biological replicates of the proximity labeling reaction were performed follow by purification of the biotinylated proteins, trypsinization, purification of peptides, TMT labeling, and detection and analysis by MS. In addition, this TMT-dataset (18-plex) contains 6 additional samples of from an independent experiment analyzing the proximity labeling of a 2xFYVE-GFP-APEX2 construct, but these samples were not included in further data analysis. We found that the DOR proximal proteome was highly enriched in endosomal proteins compared to the cytoplasmic control, and found 13 proteins significantly changed (FDR<0.1) with DNAJC13 knockdown.

2024-09-03 | PXD044921 | Pride

RNA-seq of precision cut liver slice (PCLS) culture treated with increasing amounts of alpha-linolenic acid and insulin

Project description:This experiment was designed to test the effect of alpha-linolenic acid (ALA) and insulin on liver slices prepared from Atlantic salmon. Liver slices were incubated with increasing concentrations of ALA and insulin from 20µM to 100µM and 10nM to 100nM, respectively. RNA was subsequently sequenced and response was evaluated and compared to the expected response from Atlantic salmon feeding trials. The purpose of this was to evaluate liver slice culture as a cell culture system for studying lipid metabolism in Atlantic salmon.

2019-05-08 | E-MTAB-7366 | biostudies-arrayexpress

PerTurboID of Plasmofium falciparum cytoadhesion complex

Project description:In this project proximity labeling was used to first identify proteins in the close vicinity of the P. falciparum exported kinase FIKK4.1 by fusing it to a biotin ligase. A conditional KO of the exported kinase FIKK4.1 was then generated for two identified targets, PTP4 and Kahrp in a FIKK4.1 conditional KO line. We then measured the proximity proteome of KAHRP and PTPT4 in the presence, and absence of FIKK4.1.

2023-09-21 | PXD039125 | Pride

RNA-seq, term-seq and tagRNA-seq of M. tuberculosis strains H37Rv and RhoDUC strains induced for Rho depletion at times 0H, 1.5H, 3H, 4.5H and 6H

Project description:Accurately controlled termination of transcription is critical for gene expression and adaptation to changing environments in bacteria. The aim of this study was to define transcription termination sites in Mycobacterium tuberculosis at nucleotide resolution. To this end, we used a combination of term-seq to identify termination of transcription and tagRNA-seq to identify transcription start sites and processed sites. This led us to identify a prevalence of Rho-dependent termination of transcription in the pathogen. We applied term-seq and WTSS RNA-seq on the RhoDUC strain derived from H37Rv, for which a depletion of Rho is inducible by addition of Anhydrous Tetracyclin, to identify Rho-responsive termination site and quantify readthrough.

2022-11-01 | E-MTAB-11753 | 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