Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Liver expression data from 31 mouse strains treated with vehicle or isoniazid for 3 days

ABSTRACT: Isoniazid induced varying degrees of hepatic steatosis in an inbred strain Mouse Diversity Panel (MDP) study. RNA was isolated from all animals for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive isoniazid-induced steatosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE55489 | GEO | 2014/06/03

SECONDARY ACCESSION(S): PRJNA239764

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Liver expression data from 31 mouse strains treated with vehicle or isoniazid for 3 days

Project description:Isoniazid induced varying degrees of hepatic steatosis in an inbred strain Mouse Diversity Panel (MDP) study. RNA was isolated from all animals for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive isoniazid-induced steatosis. 235 total samples from 31 strains were analyzed: N=4 per treatment and strain, except isoniazid-treated LP/J (N=3), PL/J (N=3), SM/J (N=2), NON/LtJ (N=3), LG/J (N=3), MA/MyJ (N=2), RIIIS/J (N=3), SEA/GnJ (N=2), and A/J (N=2) animals where animals that died before the completion of the study were excluded from data analysis; 13 of 31 strains exhibited findings of isoniazid-induced steatosis and were coded as responders.

2014-06-03 | E-GEOD-55489 | biostudies-arrayexpress

Liver expression data from four mouse strains treated with vehicle or PF-04287881 for seven days

2016-10-21 | GSE52620 | GEO

Liver expression data from four mouse strains treated with vehicle or PF-04287881 for seven days

Project description:PF-04287881 induced varying degrees of liver necrosis and phospholipidosis in a 34-inbred strain Mouse Diversity Panel (MDP) study. Four strains with differing susceptibilities to these phenotypes (MA/MyJ, NZW/LacJ, SM/J, WSB/EiJ) were selected for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive PF-04287881-induced liver injury. Thirty-one total samples were analyzed: N=4 per treatment and strain, except PF-04287881-treated WSB/EiJ (N=3) where one animal died before the completion of the study due to gavage error. Two strains exhibited findings of PF-04287881-induced Kupffer cell vacuolation and were coded as phospholipidosis responders (MA/MyJ and NZW/LacJ). One strain exhibited findings of single cell necrosis and was coded as a necrosis responder (NZW/LacJ).

2016-10-21 | E-GEOD-52620 | biostudies-arrayexpress

Gene expression profile of wild-type and isoniazid resistant strains of Mycobacterium smegmatis

Project description:Understanding emergence of drug resistance in pathogens systematically is a major challenge. To address this issue, lab-evolved strain resistant to first-line tuberculosis drug, isoniazid (INH), was analysed. Transcriptome analysis of different conditions revealed genes that are differentially regulated in wild-type (WT) and isoniazid resistant (2XR and 4XR) strains. Microarray analysis was performed for WT, sub-MIC, 2XR and 4XR strains of Mycobacterium smegmatis. Overall, the numbers of DEGs observed are 1529 in sub-MIC (596 - up, 933 - down), 1381 (899 – up, 482 – down) in 2XR and 716 in 4XR (267 – up, 449 – down) conditions. 52 of them are seen to be up-regulated across all drug concentrations as compared to WT while 185 are seen to be down-regulated in all. Transcriptome analysis revealed that there are variations in gene expression pattern in the resistant strains as compared to WT strain. This indicates that differential regulation of genes is, in some way, responsible for conferring the phenotype to the organism.

2014-12-13 | GSE64132 | GEO

Effect of addition of cysteine to isoniazid treatment of Mycobacterium tuberculosis

Project description:Transcriptional profiling of Mycobacterium tuberculosis H37Rv after 4 hours of combination isoniazid and cysteine treatment relative to treatment with isoniazid alone.

2017-03-27 | GSE86184 | GEO

Protein profile at different cellular fractions of Mycobacterium tuberculosis strains after exposure to Isoniazid

Project description:Out of the 10 million of tuberculosis (TB) cases estimated in the world, around 14% are isoniazid (INH) resistant among new cases and 29% among previously treated cases in the last decade. INH is one of the oldest but also one of the more potent drugs to eliminate Mycobacterium tuberculosis (Mtb), the causing agent of TB. Because of the efficiency of isoniazid (INH) against Mycobacterium tuberculosis (Mtb), many studies are still focused in better understand its role in different bacterial metabolic pathways. We recently conducted a study that evaluated the changes in the protein abundance at different cellular fractions when clonal strains of Mtb developed INH resistance in the clinical and laboratory setting. Here, we want to establish which of the protein changes occurred or started because of the initial exposure to INH. Additionally, we wanted to evaluate if those changes happen differently in strains that are sensitive or resistant to INH, evaluating different cellular compartments from two different genetic lineages of Mtb. For this purpose, we analyzed the proteome of each cellular compartment (cytosol, cell wall, membrane and secreted proteins) through liquid chromatography (nano-HPLC) coupled to mass spectrometry using the Orbitrap Velos instrument and a t-test to perform the statistical analysis for each pair comparison.

2019-06-17 | PXD007588 | Pride

Mycobacterium tuberculosis transcriptional response to Isoniazid

Project description:Mycobacterium tuberculosis transcriptional response to Isoniazid

| PRJNA694989 | ENA

Isoniazid resistant TB in South Africa

Project description:Isoniazid resistant TB in South Africa

| PRJEB67660 | ENA

Comprehensive biochemical characterization of Mycobacterium tuberculosis clonal strains after isoniazid resistance

Project description:This project describes the isoniazid (INH) resistance acquisition event in Mycobacterium tuberculosis (Mtb) from the proteomics perspective. In this way, an exploration of the protein differences, comparing clonal INH susceptible (INHs) and INHr pairs of Mtb were evaluated. One clonal clinical and one clonal laboratory-derived Mtb pair with different susceptibility profiles to INH were studied. The laboratory INHr strain had one katG mutation (V1A), while the clinical INHr strain had two (V1A and E3V). Large-scale bacterial cultures were grown in triplicate to obtain secreted proteins as well as proteins from cell fractions. The resulting peptide solutions from all fractions were analyzed using liquid-chromatography coupled with tandem mass spectrometry (LC-MS/MS). LC-MS/MS spectra were compared against an Mtb database to determine the protein abundance. Protein abundance differences were tested by Student’s t test. Looking at the same cellular fractions, there were 25 commonly altered Mtb proteins after acquiring INH resistance. These proteins were involved in ATP synthase machinery, lipid metabolism, regulatory events, virulence, detoxification and adaptation processes.

2018-06-25 | PXD009549 | Pride

Toxicoproteomic Profiling of hPXR Transgenic Mice Treated with Rifampicin and Isoniazid

Project description:Tuberculosis is a global health threat that affects millions of people every year, and treatment-limiting toxicity remains a considerable source of treatment failure. Recent reports have characterized the nature of hPXR-mediated hepatotoxicity and systemic toxicity of antitubercular drugs. The antitubercular drug isoniazid plays a role in such pathologic states as acute intermittent porphyria, anemia, hepatotoxicity, hypercoagulable states (deep vein thrombosis, pulmonary embolism, or ischemic stroke), pellagra (vitamin B3 deficiency), peripheral neuropathy, and vitamin B6 deficiency. However, the mechanisms by which isoniazid administration leads to these states are unclear. To elucidate the mechanism of rifampicin- and isoniazid-induced liver and systemic injury, we performed tandem mass tag mass spectrometry-based proteomic screening of mPxr–/– and hPXR mice treated with combinations of rifampicin and isoniazid. Proteomic profiling analysis suggested that the hPXR liver proteome is affected by antitubercular therapy to disrupt [Fe–S] cluster assembly machinery, [2Fe–2S] cluster-containing proteins, CYP450 enzymes, heme biosynthesis, homocysteine catabolism, oxidative stress responses, vitamin B3 metabolism, and vitamin B6 metabolism. These findings provide insight into the etiology of some of these processes and potential targets for subsequent investigations.

2020-07-19 | PXD019505 | Pride

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