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Profiling of differential RNAs in alpha amanitin treated SORBS2-depleted ovarian cancer cells and control-treated SORBS2-depleted

ABSTRACT: In this study, we examined the differential RNA profile of alpha amanitin-treated SORBS2-depleted ovarian cancer cells compared with control-treated SORBS2-depleted cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE101595 | GEO | 2018/02/20

REPOSITORIES: GEO

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Profiling of differential RNAs in SORBS2-depleted ovarian cancer cells and control cells

Project description:In this study, we examined the differential RNA profile of SORBS2-depleted ovarian cancer cells compared with control cells

2018-02-20 | GSE101594 | GEO

Alpha-amanitin treatment effect on intronic transcription

Project description:We compared the gene expression profiles of prostate carcinoma cells, LNCaP, treated or not with an inhibitor of RNA Polymerase II (RNAP II), alpha-amanitin. These experiments pointed to a fraction of intronic messages that seems to be insensitive to alpha-amanitin or up-regulated in cells with blocked RNAP II transcription. Keywords: RNA-polymerase II inhibition experiments

2007-03-29 | GSE5453 | GEO

Homo sapiens

Project description:Profiling of differential RNAs in alpha amanitin treated SORBS2-depleted ovarian cancer cells and control-treated SORBS2-depleted

| PRJNA394908 | ENA

RNA expression analysis after RNA polymerase II transcriptional blocking with α-amanitin

Project description:Transcriptional profiling of HeLa cells treated with α-amanitin for 9 h. Relative abundance to untreated control cells was used to evaluate the biogenesis of lncRNAs by RNA polymerase II. Two-condition experiment, alpha-amanitin-treated vs. untretated HeLa cells. Biological replicates: 4 with dye-swap

2015-06-30 | E-GEOD-62989 | biostudies-arrayexpress

RNA expression analysis after RNA polymerase II transcriptional blocking with α-amanitin

2015-06-30 | GSE62989 | GEO

Genome-wide CRISPR loss-of-function screen for α-amanitin

Project description:The “death cap”, Amanita phalloides, is the world’s most poisonous mushroom, responsible for 90% of mushroom-related fatalities. The most fatal component of the death cap is α-amanitin(AMA). Despite its lethal effect, the exact mechanisms of how α-amanitin poisons humans remain unclear, leading to no specific antidote available for treatment. Here, we performed a genome-wide CRISPR loss-of-function screen to identify genes and pathways involved in AMA cytotoxicity.

2023-03-07 | GSE226447 | GEO

Transcription profiling of Xenopus laevis early gastrulation embryos injected with alpha-amanitin against RNA polymerase II activity

Project description:Xenopus laevis embryos were injected with alpha-amanitin to inhibit RNA polymerase II activity. Embryos were allowed to develop up to stage 10.5 (early gastrula, control and alpha-amanitin injected embryos) and subsequently collected for RNA isolation. The transcriptome profiles of alpha-amanitin injected and control embryos were compared.

2016-03-07 | E-MTAB-3614 | biostudies-arrayexpress

The Mechanisms Underlying α-Amanitin Resistance in Drosophila melanogaster: A Microarray Analysis

Project description:The rapid evolution of toxin resistance in animals has important consequences for the ecology of species and our economy. Pesticide resistance in insects has been a subject of intensive study, however, very little is known about how Drosophila species became resistant to natural toxins with ecological relevance, such as α-amanitin that is produced in deadly poisonous mushrooms. Here we performed a microarray study to elucidate the genes, chromosomal loci, molecular functions, biological processes, and cellular components that contribute to the α-amanitin resistance phenotype in Drosophila melanogaster. We suggest that toxin entry blockage through the cuticle, phase I and II detoxification, sequestration in lipid particles, and proteolytic cleavage of α-amanitin contribute in concert to this quantitative trait. We speculate that the resistance to mushroom toxins in Drosophila melanogaster and perhaps in mycophagous Drosophila species has evolved as a cross-resistance to pesticides or other xenobiotic substances.

2015-12-01 | GSE52782 | GEO

The NTCP receptor inhibitor Ezetimibe reduces the toxicity of α-amanitin: in vitro and in vivo study.

Project description:Background and Aims: To verify the protective effect of Ezetimibe, an sodium taurocholate co-transporting polypeptide (NTCP) inhibitor, on α-amanitin poisoning in vitro and in vivo by inhibiting NTCP to prevent α-amanitin into hepatocytes. Approach and Results: In animal experiments, the survival rate was significantly improved in the treatment group. The pathomorphological characteristics of liver and kidney in the treatment group were significantly improved. In cell experiments,The cell viability of the treatment group was significantly improved, and the expression of NTCP in the treatment group was significantly decreased by immunofluorescence. In molecular docking simulations, we demonstrated the potential of NTCP to bind Ezetimibe and α-amanitin, respectively. Transcriptomics in high-throughput sequencing was used to detect the differential metabolic genes between α-amanitin poisoning group and the treatment group, and signal pathway enrichment was used to analyze the significantly different signal pathways. Conclusions: Ezetimibe, as an inhibitor of NTCP, can reduce the entry of α-amanitin into hepatocytes to play a protective role and improve the cell viability and survival rate of mice.

2023-06-30 | GSE235740 | GEO

Expression data for MCF-7 treated with PolII inhibitors, Triptolide or alpha-amanitin

Project description:Transcription of mRNA in mammalian is mainly performed by RNA polymerase II (PolII). POLRMT is responsible for the production of cytoplasmic and nuclear form of mitochondrial RNA polymerase. The former (mtRNAP) participates in transcription of RNA in the mitochondria while the latter (spRNAP-IV) is responsible for some mRNA transcription in the nucleus. The nature and amount of genes transcribed by spRNAP-IV still remains unclear. Thus, we scanned for possible candidate genes by using Affymetrix. MCF7 cells were cultured in RPMI medium supplemented with 10% fetal bovine serum. To determine the inhibition of PolII transcription, cells were cultured in the presence of 10 μg/ml of alpha-amanitin or 0.3μM of triptolide (Sigma) for 48 or 24 h, respectively.

2011-07-01 | E-GEOD-28444 | biostudies-arrayexpress

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