Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: mouse oral and hepatic metagenome

PROVIDER: PRJNA803949 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17902820_subreads.fastq.gz	Fastqsanger.gz
	SRR17902821_subreads.fastq.gz	Fastqsanger.gz
	SRR17902822_subreads.fastq.gz	Fastqsanger.gz
	SRR17902823_subreads.fastq.gz	Fastqsanger.gz
	SRR17902824_subreads.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 21

Similar Datasets

Project description:mouse oral metagenome

| PRJNA793991 | ENA

Serial gene expression profiling in the liver of Pdgf-c Tg mice that developed hepatic fibrosis and tumors

2012-10-03 | GSE31431 | GEO

Serial gene expression profiling in the liver of Pdgf-c Tg mice that developed hepatic fibrosis and tumors

Project description:Over expression of PDGF-C in mouse liver resulted in the progression of hepatic fibrosis, steatosis and the development of HCC; this mouse model closely resembles the human HCC that is frequently associated with hepatic fibrosis. Peretinoin (generic name; code, NIK-333), developed by the Kowa Company, (Tokyo, Japan), is an oral acyclic retinoid (ACR) with a vitamin A-like structure that targets the retinoid nuclear receptor. Peretinoin effectively inhibits the progression of hepatic fibrosis and tumors in Pdgf-c Tg mice. Gene expression profiling was evaluated during the progression of hepatic fibrosis and tumors. After weaning at week 4, Pdgf-c Tg or non-transgenic WT mice were fed a basal diet or a diet containing+0.06% peretinoin respectively. At week 20, mice were sacrificed for the analysis of progression of hepatic fibrosis. At week 48, mice were sacrificed for the analysis of the development of hepatic tumors.

2012-10-03 | E-GEOD-31431 | biostudies-arrayexpress

Mouse associated oral microbiome

Project description:Mouse associated oral microbiome Metagenome

| PRJNA521993 | ENA

Changes in Hepatic Gene Expression upon Oral Administration of Taurine-Conjugated Ursodeoxycholic Acid in ob/ob Mice

Project description:We examined the effect of oral TUDCA treatment on hepatic steatosis and associated changes in hepatic gene expression in ob/ob mice.

2010-12-31 | GSE22608 | GEO

Defining the Secrebiome: the expressed secretome of the gut microbiome and its role in obese Mexican children

Project description:high throughput sequencing of the metagenome of mexican children

2020-03-16 | GSE143207 | GEO

Modulating the gut microbiota by dietary guar gum protects against diet-induced obesity but promotes non-alcoholic steatohepatitis in mice

Project description:Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming the most common liver disease worldwide, yet the pathogenesis of NAFLD is only partially understood. Here, we investigated the role of the gut bacteria in NAFLD by stimulating the gut bacteria via feeding mice the fermentable dietary fiber guar gum and suppressing the gut bacteria via chronic oral administration of antibiotics. Guar gum feeding profoundly altered the gut microbiota composition, in parallel with reduced diet-induced obesity and improved glucose tolerance. Strikingly, despite reducing adipose tissue mass and inflammation, guar gum enhanced hepatic inflammation and fibrosis, concurrent with markedly elevated plasma and hepatic bile acid levels. Consistent with a role of elevated bile acids in the liver phenotype, treatment of mice with taurocholic acid stimulated hepatic inflammation and fibrosis. In contrast to guar gum, chronic oral administration of antibiotics effectively suppressed the gut bacteria, decreased portal secondary bile acid levels, and attenuated hepatic inflammation and fibrosis. Neither guar gum or antibiotics influenced plasma lipopolysaccharide levels. In conclusion, our data indicate a causal link between changes in gut microbiota and hepatic inflammation and fibrosis in a mouse model of NAFLD, possibly via alterations in bile acids.

2017-06-06 | GSE76087 | GEO

Changes in Hepatic Gene Expression upon Oral Administration of Taurine-Conjugated Ursodeoxycholic Acid in ob/ob Mice

Project description:We examined the effect of oral TUDCA treatment on hepatic steatosis and associated changes in hepatic gene expression in ob/ob mice. We administered TUDCA to ob/ob mice at a dose of 500 mg/kg twice a day by gastric gavage for 3 weeks. Body weight, glucose homeostasis, endoplasmic reticulum (ER) stress, and hepatic gene expression were examined in comparison with control ob/ob mice and normal littermate C57BL/6J mice.

2010-12-31 | E-GEOD-22608 | biostudies-arrayexpress

Genome-wide profiling of LXR, RXR and PPARM-NM-1 in mouse liver reveals extensive sharing of binding sites

Project description:The liver X receptors (LXRs) are nuclear receptors that form permissive heterodimers with retinoid X receptor (RXR) and are important regulators of lipid metabolism in the liver. We have recently shown that RXR agonist-induced hypertriglyceridemia and hepatic steatosis in mice is dependent on LXR and correlates with an LXR-dependent hepatic induction of lipogenic genes. To further investigate the role of RXR and LXR in the regulation of hepatic gene expression, we have mapped the ligand-regulated genome-wide binding of these factors in mouse liver. We find that the RXR agonist bexarotene primarily increases the genomic binding of RXR, whereas the LXR agonist T0901317 greatly increases both LXR and RXR binding. Functional annotation of putative direct LXR target genes revealed a significant association with classical LXR-regulated pathways as well as PPAR signaling pathways, and subsequent ChIP-seq mapping of PPARM-NM-1 binding demonstrated binding of PPARM-NM-1 to 71-88% of the identified LXR:RXR binding sites. Sequence analysis of shared binding regions combined with sequential ChIP on selected sites indicate that LXR:RXR and PPARM-NM-1:RXR bind to degenerate response elements in a mutually exclusive manner. Together our findings suggest extensive and unexpected cross-talk between hepatic LXR and PPARM-NM-1 at the level of binding to shared genomic sites LXR, RXR, PPARalpha and RNA Polymerase II ChIP-seq on livers from female C57BL/6 wild-type and/or LXRM-NM-1/M-NM-2-deficient mice (13 weeks of age, n=1) treated by oral gavage once daily for 14 days with the RXR agonist bexarotene (100 mg/kg body weight [mpk], in 1% carboxymethylcellulose), the LXR agonist T0901317 (T09, 30 mpk) or vehicle alone.

2012-01-31 | E-GEOD-35262 | biostudies-arrayexpress

Antibiotic-induced acceleration of type 1 diabetes alters maturation of innate intestinal immunity

Project description:The early-life intestinal microbiota plays a key role in shaping host immune system development. We found that a single early-life antibiotic course (1PAT) accelerated Type 1 diabetes (T1D) development in male NOD mice. The single course had strong and persistent effects on the intestinal microbiome, selecting for a highly metabolically active metagenome, with altered hepatic and serum metabolites. The exposure led to differential ileal and hepatic histone modification, and perturbed ileal gene expression, strongly affecting the normal maturational pattern. Earliest effects involved specific genes in innate immune pathways, with later effects on adaptive immunity. Microbiome analysis revealed four potential T1D-protective taxa and four T1D-accelerating taxa, and a network linking specific microbial taxa to differences in ileal gene expression was identified. This simplified animal model has improved understanding of the mechanisms by which early-life gut microbiome perturbations alter host intestinal responses, contributing to T1D.

2018-08-03 | GSE101721 | 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