Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47148 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6558310_1.fastq.gz | Fastqsanger.gz | |||
| ERR6558310_2.fastq.gz | Fastqsanger.gz | |||
| ERR6558311_1.fastq.gz | Fastqsanger.gz | |||
| ERR6558311_2.fastq.gz | Fastqsanger.gz | |||
| ERR6558312_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:Microbial community of a chlordecone contaminated nitisol subject to a remediation process based on chemical reduction
| PRJEB9579 | ENA
Project description:Exposure to pesticide chlordecone is associated with high risk of prostate cancer.We hypothesised that changes in histone H3K4me3 could be involved in pathological processes in prostate induced by chlordecone. We exposed mice to chlordecone during embryonic development (E6.5-E15.5) and we analysed F1 progeny male epigenetic H3K4me3 marks in prostate tissue, as well as H3K4me3 in the prostate of F3 progeny to reveal the transgenerational effects resulting from the ancestral exposure to CD. We performed ChIP using H3K4me3 commercial antibody (Merck Millipore, 07-473) and pooled prostate tissues from 4 mice. DNA-protein complex was immunoprecipitated, eluted and DNA purified.
2021-04-01 | GSE135199 | GEO
Project description:We hypothesized that gestational exposure to chlordecone can lead to alteration of murine ovary's epigenetic landscape. To test our hypothesis, we exposed mice to chlordecone during embryonic development and we analyzed F1 female progeny epigenetic mark H3K4me3 in ovaries. We performed ChIP using anti-H3K4me3 commercial antibody (Merck Millipore, 07-473). DNA-protein complexes were immunoprecipitated, eluted and then DNA were purified.
2019-05-21 | GSE129897 | GEO
Project description:Selective, efficient, and controllable oxidation of cytosine modifications is valuable for epigenetic analyses, yet only limited progress has been made. Here, we present two modular chemical oxidation reactions: conversion of 5-hydroxymethylcytosine (5hmC) into 5-formylcytosine (5fC) utilizing 4-acetamido-2,2,6,6-tetramethylpiperidine-1-oxoammonium tetrafluoroborate (ACT+ BF4–) and further transformation of 5fC into 5-carboxycytosine (5caC) through Pinnick oxidation. Both reactions are mild and efficient on double-stranded DNA. We integrated these two oxidations with borane reduction to develop chemical-assisted pyridine borane sequencing plus (CAPS+), for direct and quantitative mapping of 5hmC. Compared with chemical-assisted pyridine borane sequencing (CAPS), CAPS+ improved the conversion rate and false-positive rate. We applied CAPS+ to mouse embryonic stem cells (mESCs) DNA, human normal brain and glioblastoma DNA samples, and demonstrated its superior sensitivity in analyzing the hydroxymethylome
2023-03-15 | GSE214006 | GEO
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:RNA seq project designed to understand the role of pesticide on transription of mRNA in the testis. We treated adult female mice with chlordecone with doses 0 (control), 100 Xg/kg/day and 1 mg/kg/day during gestation period E6- E15. Male born from Chlordecone- treated mice were crossed for a three generations. The testes from F3 generations were taken for mRNA extraction. For mRNA extraction we used columb. Three biological replicates used for each condition . We hypothesize that chlordecone cause changes in mRNA due to transgenerational effect of pesticides (Skinner et al, Science 2005). The changes in expression of certain genes can help us understand the effect of pesticides on many tissues. Number of sample :9 samples. We require Paired End sequencing and number of reads equal or more than 25M tags, strand specific sequencing
2018-07-10 | GSE86438 | GEO
Project description:Pyridoxal phosphate (PLP) is an enzyme cofactor required for the chemical transformation of biological amines in numerous essential cellular processes. PLP-dependent enzymes (PLP-DEs) are ubiquitous and evolutionarily diverse, making their classification based on sequence homology challenging. This calls for a more direct approach for identifying new PLP-DEs and uncovering novel roles of PLP within the cell. We present a chemical proteomic method for reporting on PLP-DEs using functionalized cofactor probes. PL-analogs designed to be taken up by cells and metabolized in situ were synthesized. The probes are phosphorylated to functional cofactor surrogates by cellular PL kinases and bind to PLP-DEs via a reversible aldimine bond, which can be fixed by NaBH4-reduction. Conjugation to a reporter tag permits the identification of PLP-DEs using quantitative, label-free mass spectrometry via confidence ranking and profile searches. We label a significant portion of the PLP-ome in Staphylococcus aureus (41%) and annotate uncharacterized proteins as novel PLP-DEs. In applying our method, we were able to study structural tolerance within PLP-DE active sites and to screen for off-targets of the PLP-DE inhibitor D-cycloserine. Our cofactor profiling method represents a robust way to mine the cellular inventory of PLP-DEs which can be used for genome annotation, comparative profiling and drug development.
2018-10-17 | PXD006483 | Pride
Project description:Chlordecone (CLD) is a pesticide used to control the banana weevill in the French West Indies from 1970 to 1993. Despite its ban in the 90s, the highly persistence of CLD and contamination of the food webs raised tremendous concern for public health [1]. CLD can induce reprotoxic, neurotoxic and hepatotoxic effects in humans and is involved in prostate cancer [2] and liver fibrosis potentiation [3]. In liver, although CLD is metabolized into phase I metabolite chlordecol (CLD-OH), it is highly biopersistent. Nevertheless, the cellular hepatic effects of these 2 compounds have been poorly described. Therefore, we used an original approach to investigate in vitro toxicity responses of CLD and CLD-OH in liver cell models (HepaRG cells and primary human hepatocytes, PHHs) using metabolomics and proteomics. 1) Resiere, D., et al. (2023). Chlordecone (Kepone) poisoning in the French Territories in the Americas. Lancet 401, 916. 2) Multigner L., et al. (2010). Chlordecone exposure and risk of prostate cancer. J Clin Oncol 28, 3457-3462. 3) Tabet E., et al. (2016). Chlordecone potentiates hepatic fibrosis in chronic liver injury induced by carbon tetrachloride in mice. Toxicol Lett 255, 1-10.
2025-06-10 | PXD043683 | Pride