Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274497 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:At 2 months of age, liver-specific insulin receptor knockout (LIRKO) mice present hyperglycemia and hyperinsulinemia. Furthermore, LIRKO mice have increased levels of hepatic cholesterol. Indeed, many changes seen in cholesterol metabolism in LIRKO mice are also observed in humans with metabolic syndrome. For example, both show decreased levels of HDL and increased secretion of apoB and VLDL. These findings make the LIRKO mouse a unique non-dietary model of insulin resistant, hyperglycemia, dyslipidemia and atherosclerosis that resembles several clinical features of the human metabolic syndrome. By hepatic transcriptomic analysis of the wild-type (WT) offspring of LIRKO mice, we identify that members of the TGF-β family are differentially expressed in the offspring, including the NREP and GDF15.
2021-01-04 | GSE141077 | GEO
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
2014-12-04 | GSE61417 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility. Gene expression was measured in whole testis from males aged 62-86 days. Samples include 190 first generation lab-bred male offspring of wild-caught mice from the Mus musculus musculus - M. m. domesticus hybrid zone.
2014-12-04 | E-GEOD-61417 | biostudies-arrayexpress
Project description:To characterize the genetic basis of hybrid male sterility in detail, we used a systems genetics approach, integrating mapping of gene expression traits with sterility phenotypes and QTL. We measured genome-wide testis expression in 305 male F2s from a cross between wild-derived inbred strains of M. musculus musculus and M. m. domesticus. We identified several thousand cis- and trans-acting QTL contributing to expression variation (eQTL). Many trans eQTL cluster into eleven ‘hotspots,’ seven of which co-localize with QTL for sterility phenotypes identified in the cross. The number and clustering of trans eQTL - but not cis eQTL - were substantially lower when mapping was restricted to a ‘fertile’ subset of mice, providing evidence that trans eQTL hotspots are related to sterility. Functional annotation of transcripts with eQTL provides insights into the biological processes disrupted by sterility loci and guides prioritization of candidate genes. Using a conditional mapping approach, we identified eQTL dependent on interactions between loci, revealing a complex system of epistasis. Our results illuminate established patterns, including the role of the X chromosome in hybrid sterility.
2014-05-01 | GSE54089 | GEO
Project description:Gene expression in liver-specific insulin receptor knockout (LIRKO) and IR/FoxO1 double knockout (LIRFKO) mice
| PRJNA256986 | ENA
Project description:Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before the acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin and hepatic cell necrosis. Moreover, LcS alleviated the acetaminophen-induced intestinal mucosal permeability, elevation in serum IL-1α and lipopolysaccharide, and decreased levels of serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria, Oxyphotobacteria, long-chain fatty acids, cholesterol and sugars in the gut. Additionally, the transcriptome and proteomics showed that LcS mitigated the downregulation of metabolism and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS.
2023-07-26 | PXD044099 |
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:Hepatic gene expression data from cadmium-exposed mice
| PRJNA325601 | ENA
Project description:Hepatic gene expression profiling in AHNAK KO mice
| PRJNA287673 | ENA