Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31911212_1.fastq.gz | Fastqsanger.gz | |||
| SRR31911212_2.fastq.gz | Fastqsanger.gz | |||
| SRR31911213_1.fastq.gz | Fastqsanger.gz | |||
| SRR31911213_2.fastq.gz | Fastqsanger.gz | |||
| SRR31911214_1.fastq.gz | Fastqsanger.gz |
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Project description:The effect of krill powder, a mixed source of protein and n-3 PUFAs from Antarctic Krill (Euphausia superba), on hepatic gene expression was analyzed in CBA/J mice. Mice were fed a low-fat control diet or a 3% (w/w) krill powder low-fat diet for three months. Gene expression profiling on liver samples revealed that the krill powder supplemented diet modulated a large number of pathways compared to the control diet, and we focused on the genes involved in metabolic processes. Pathways involved β-oxidation, glucose metabolism, and amino acid catabolism were downregulated. In contrast, genes involved in the mitochondrial electron transport chain were upregulated. Thus, a krill powder supplemented diet had potent and specific effects on energy metabolism and oxidative phosphorylation at the gene level. This indicates that krill powder supplementation could be an approach to prevent age-related decline in mitochondrial respiratory chain function and weight loss.
2021-11-25 | GSE46049 | GEO
Project description:In this study, transcriptome technology was used to explore the mechanism of Poecilobdella manillensis lyophilized powder to improve the inflammatory injury of rat mesangial cells.In general, this study found that TXNIP / NLRP3 signaling pathway is one of the effective mechanisms of Poecilobdella manillensis lyophilized powder to improve the inflammatory injury of diabetic nephropathy.
2024-10-09 | GSE270526 | GEO
Project description:The breakdown of oomycete necromass is an important source of organic matter for composting. How Trichoderma harzianum, an important composting fungus, regulates gene expression and produces exo-proteins for degradation of oomycete necromass is poorly understood, especially related to cellulose, an important component of oomycete necromass. Complementary techniques of chemical compositional analysis, transcriptomics, exo-proteomics, enzymatic assays, and fungal genetics were used to analyze the degradation of inactivated oomycete mycelial powder – a surrogate for oomycete necromass. In total, 1,556 genes were upregulated and 212 exo-proteins were produced in T. harzianum oomycete mycelial powder cultures, and about 25% of the produced proteins showed corresponding gene upregulation. The enzymes detected, such as β-1,3-glucanases, and β-1,4-glucanases (cellulases), matched well with the composition of oomycete mycelial powder. Linkage compositional analysis showed that the mycelial powder contained ~ 60% 1,3 linkages and ~19% 1,4 linkages. The enzyme cocktail from the submerged cultures converted approximately one-third of the mycelial powder to glucose by in vitro assays. The conversion of the mycelial powder to glucose was not substantially reduced by deletion of the cellulolytic transcriptional activator XYR1. Deletion of XYR1 did decrease cellulase activity but only ~1% of mycelial powder-induced genes appeared to be XYR1-regulated. In conclusion, T. harzianum produces suitable enzyme cocktails for oomycete mycelial powder degradation, with β-1,3-glucanases likely playing a more important role than cellulases. T. harzianum cellulases may either be relatively unimportant for the degradation, or may not be co-activated alongside CAZymes degrading less recalcitrant parts of the mycelial powder.
2025-10-11 | PXD069347 | Pride
Project description:While the paradigm that genetic predisposition and environmental exposures interact to shape development and function of the human brain and ultimately the risk of psychiatric disorders has drawn wide interest, the corresponding molecular mechanisms have not been elucidated yet. Here we show that a functional polymorphism altering chromatin interaction between the transcription start site and long range enhancers in the FK506 binding protein 5 (FKBP5) gene, an important regulator of the stress hormone system, increases the risk of developing stress-related psychiatric disorders in adulthood by allele-specific, childhood trauma-dependent DNA demethylation in functional glucocorticoid response elements (GREs) of FKBP5. This demethylation is linked to increased stress-dependent gene transcription followed by a long-term dysregulation of the stress hormone system and a global impact on the function of immune cells and brain areas associated with stress regulation. This first identification of molecular mechanisms of genotype-directed long-term environmental reactivity will also critically contribute to designing more effective treatment strategies for stress-related disorders. Effects of FKBP5 rs1360780 genotype x environment interaction on peripheral blood mRNA expression of GR responsive genes, as measured by gene expression arrays, were explored in 129 individuals (child abuse/risk allele carrier N = 40, child abuse/protective allele carrier N = 15; and no child abuse/risk allele carrier N = 60, no child abuse/protective allele carrier N = 14).
2012-11-03 | GSE42002 | GEO
Project description:While the paradigm that genetic predisposition and environmental exposures interact to shape development and function of the human brain and ultimately the risk of psychiatric disorders has drawn wide interest, the corresponding molecular mechanisms have not been elucidated yet. Here we show that a functional polymorphism altering chromatin interaction between the transcription start site and long range enhancers in the FK506 binding protein 5 (FKBP5) gene, an important regulator of the stress hormone system, increases the risk of developing stress-related psychiatric disorders in adulthood by allele-specific, childhood trauma-dependent DNA demethylation in functional glucocorticoid response elements (GREs) of FKBP5. This demethylation is linked to increased stress-dependent gene transcription followed by a long-term dysregulation of the stress hormone system and a global impact on the function of immune cells and brain areas associated with stress regulation. This first identification of molecular mechanisms of genotype-directed long-term environmental reactivity will also critically contribute to designing more effective treatment strategies for stress-related disorders. Effects of FKBP5 rs1360780 genotype x environment interaction on peripheral blood mRNA expression of GR responsive genes, as measured by gene expression arrays, were explored in 129 individuals (child abuse/risk allele carrier N = 40, child abuse/protective allele carrier N = 15; and no child abuse/risk allele carrier N = 60, no child abuse/protective allele carrier N = 14). In all 129 individuals, 1627 transcripts showed a significant correlation with plasma cortisol concentrations, suggesting their GR responsiveness. The correlation of 76 of these transcripts with cortisol plasma levels showed significant differences when stratifying by FKBP5 genotype in individuals with child abuse (Fisher z score ≥ 1.96) For these 76 transcripts, the mean absolute correlation coefficient with plasma cortisol was R = 0.23 in the risk allele carriers with child abuse, that is those exhibiting a demethylation of FKBP5 intron 7 as compared to R = 0.74 in the carriers of the protective genotype with child abuse where intron 7 methylation remains largely stable. This indicates a relative GR-resistance in the trauma exposed FKBP5 risk allele vs. protective genotype carriers. These 76 transcripts did not show a genotype-dependent difference in correlation coefficients in non-trauma exposed individuals suggesting that exposure to early trauma enhances FKBP5 genotype-dependent effect of GR sensitivity, most likely by epigenetic mechanisms. These findings suggest that the combination of FKBP5 risk allele carrier status and early trauma exposure alters the stress hormone-dependent regulation of several genes in peripheral blood cells, and might thereby enhance the reported association of early trauma with immune and inflammatory dysregulation, further promoting system-wide symptoms of stress-related disorders.
2012-11-03 | E-GEOD-42002 | biostudies-arrayexpress