Aspergillus terreus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| AABT01.dat.gz | Other | |||
| AABT01.fasta.gz | Fasta.gz | |||
| AABT01.master.dat | Other | |||
| AAJN01.dat.gz | Other |
Items per page: 5 1 - 5 of 54 |
Similar Datasets
Project description:The filamentous fungus Aspergillus fumigatus is the cause of a variety of pulmonary infections (chronic pulmonary aspergillosis) and life-threatening systemic infection that can infect a variety of different organs (invasive aspergillosis). A. fumigatus is widely distributed in the environment and produces large numbers of small conidia that are inhaled daily. A rapid immune response eliminates these in the immunocompetent host but in cases of pulmonary disease or immunosuppression conidia can quickly germinate and grow in the body. Statins interfere with biosynthesis of cholesterol and are therefore used in treatment of hypercholesterolemia. There is increasing evidence for the potential use of statins in preventing and treating fungal infections. The aim of this study was to assess the effect of statins on A fumigatus and to characterize the proteomic alterations occurring in A. fumigatus in response to statin. Pre-growth of A fumigatus in the presence of statin resulted in lower levels of ergosterol. Cells also showed increased permeability as measured by elevated amino acid and protein leakage. Gliotoxin release increased about nine fold in atorvastatin treated cells. Proteomic analysis revealed differential abundance of proteins involved in oxidative stress response such as glutathione S-transferase family protein (8.43 fold increase) and heat shock protein Hsp30/Hsp42 (2.02 fold increase). Protein related to secondary metabolite biosynthesis like nonribosomal peptide synthetase fmpE (3.06 increase) and 3- Aflatoxin B1-aldehyde reductase GliO-like (-2.86 fold decrease) These results indicate that statins have the ability to reduce the growth of A. fumigatus.
2021-09-08 | PXD015254 | Pride
Project description:Filamentous fungus that produces aflatoxin and causes aspergillosis
| PRJNA12888 | ENA
Project description:With particular emphasis on interactions between cholesterol homeostasis and drug metabolism we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear receptor PXR. Expression profiling with Affymetrix whole genome arrays shows that statins induce extensive transcriptome changes. 7 condition experiment: 3 treatments (atorvastatin, rifampicin, rosuvastatin), each measured at 2 time points (24 and 48 hours), and untreated cells. 4-6 biological replicates for each condition.
2011-09-04 | E-GEOD-24187 | biostudies-arrayexpress
Project description:With particular emphasis on interactions between cholesterol homeostasis and drug metabolism we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear receptor PXR. Expression profiling with Affymetrix whole genome arrays shows that statins induce extensive transcriptome changes.
2011-09-05 | GSE24187 | GEO
Project description:With particular emphasis on interactions between cholesterol homeostasis and drug metabolism we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear receptor PXR. Expression profiling with dedicated Steroltalk cDNA arrays shows that statins induce extensive transcriptome changes.
2011-09-05 | GSE24186 | GEO
Project description:The statin family of cholesterol-lowering drugs was shown to influence the risk of multiple types of cancers. However, the anti-tumor effects of statins in pancreatic cancer and their efficacy differs among the individual statins, are not currently well-defined. Thus, the aim of the present study was to identify the biological pathways affected by individual statins in human pancreatic cancer. The study was performed on human pancreatic cancer cell linesMiaPaCa-2 and PANC-1, exposed to three statins (Lovastatin, Fluvastatin and Simvastatin). mRNA-seq were performed (Sequenced with PE150, and 20M reads were generated.)
2020-04-30 | GSE149566 | GEO
Project description:Oncogenic transformation alters the metabolism of cellular lipids to sustain tumor growth. We define a reciprocal mechanism by which cholesterol metabolism controls the formation and differentiation of pancreatic ductal adenocarcinoma (PDAC). Disruption of distal cholesterol biosynthesis by conditional inactivation of Nsdhl, or treatment with cholesterol-lowering statins caused murine pancreatic carcinomas induced by KrasG12D expression and homozygous Trp53 loss to undergo a differentiation switch from a glandular to basal (mesenchymal) phenotype. In parallel, PDACs from patients receiving statins had enhanced mesenchymal features. Mechanistically, statins and NSDHL loss induced sterol response element binding protein 1 (SREBP1), promoting autocrine transforming growth factor beta (TGF) signaling, inducing epithelial-mesenchymal transition. Activation of promesenchymal TGFβ effectors by cholesterol-lowering statins may select for poorly differentiated carcinomas.
2020-08-14 | GSE156210 | GEO
Project description:With particular emphasis on interactions between cholesterol homeostasis and drug metabolism we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear receptor PXR. Expression profiling with dedicated Steroltalk cDNA arrays shows that statins induce extensive transcriptome changes. 10 condition experiment: 3 treatments (atorvastatin, rifampicin, rosuvastatin), each measured at 3 time points (12, 24 and 48 hours), and untreated cells. 3-7 biological replicates for each treatment condition, 20 biological and technical replicates for untreated cells. Common reference design.
2011-09-04 | E-GEOD-24186 | biostudies-arrayexpress
Project description:Hantavirus causes two kinds of acute diseases; hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), and it is still a major health concern due to high mortality and lack of effective treatment. Interferon is only effective to inhibit hantavirus infection at a very early stage. Several interferon-stimulated genes (ISGs) have been indicated to inhibit hantavirus infection. The cholesterol 25-hydroxylase (CH25H) has been indicated as an ISG, which encodes an enzyme that catalyzes the production of 25-hydroxycholesterol (25HC). 25HC plays an important role in regulating cholesterol biosynthesis and inhibits multiple enveloped virus infections. Here, we showed that Hantaan virus (HTNV), the prototype hantavirus, induces CH25H in infected cells. Overexpression of CH25H and treatment of its enzymatic product 25HC both inhibit HTNV infection, possibly through lowering 3-hydroxy-3-methyl-glutaryl coenzyme A reductase regulation (HMG-CoA reductase, HMGCR) that inhibit cholesterol synthesis. Additionally, cholesterol lowering drugs, HMGCR-targeting statins process potent hantavirus inhibition effects. Taken together, our results indicate that the 25HC and statins were potential antivirals against hantavirus infection.
2024-06-27 | GSE252127 | GEO