Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529550 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8797411_1.fastq.gz | Fastqsanger.gz | |||
| SRR8797411_2.fastq.gz | Fastqsanger.gz | |||
| SRR8797412_1.fastq.gz | Fastqsanger.gz | |||
| SRR8797412_2.fastq.gz | Fastqsanger.gz | |||
| SRR8797413_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:RNA from stem containing first node and internodes during dough stage was considered for the above purpose. Satabdi, (popularly known as Minikit) most popular cultivar of West Bengal and Palman, another high yielding variety were considered for microarray analysis for comparison to each other. Two rice genotypes were grown in identical conditions (same field with contaminated ground water) to obtain the most meaningful conclusion. Dough stage was considered as variation in arsenic accumulation among the genotypes starts during dough stage to maturity. Plant tissues were collected from stem for transcriptomic analysis as expression profiling of such tissue in response to arsenic would be most useful as arsenic transport/loading in grain was assumed to be controlled by arsenic translocation behavior at inter vascular level or from xylem to phloem. Satabdi accumulates more than twice of arsenic in brown rice (0.346 mg/kg) than that of Palman (0.156 mg/kg) whereas accumulation in straw (2.07 mg/kg) was approximately less than half of the Palman (4.491 mg/kg)
2014-01-17 | E-MTAB-2106 | biostudies-arrayexpress
Project description:Chronic exposure to arsenic is associated with dermatological and non-dermatological disorders. Consumption of arsenic contaminated drinking water results in accumulation of arsenic in liver, spleen, kidneys, lungs and gastrointestinal tract. Although, arsenic is cleared from these sites, a substantial amount of residual arsenic is left in keratin-rich tissues such as skin. Epidemiological studies on arsenic suggest the association of skin cancer upon arsenic exposure, however, the exact mechanism of arsenic induced carcinogenesis is not completely understood. We have developed a cell line-based model to understand the molecular mechanisms involved in arsenic mediated toxicity and carcinogenicity. Human skin keratinocyte cell line, HaCaT was exposed to 100nM sodium arsenite for six months. We observed an increase in the basal ROS levels in arsenic exposed cells along with the increase in anti-apoptotic proteins. SILAC-based quantitative proteomics approach resulted in the identification and quantitation of 2,181 proteins of which 39 proteins were found to be overexpressed (≥2-fold) and 56 downregulated (≤2-fold) upon chronic arsenic exposure. Our study provides comprehensive insights into the molecular basis of chronic arsenic exposure on skin.
2017-01-02 | PXD001645 | Pride
Project description:Arsenic exposure is a global health problem. Millions of people encounter arsenic through contaminated drinking water, consumption, and inhalation. The arsenic response locus in budding yeast is responsible for the detoxification of arsenic and its removal from the cell. This locus constitutes a conserved pathway ranging from prokaryotes to higher eukaryotes. The goal of this study was to identify how the arsenic response locus is regulated in an arsenic dependent manner. An affinity enrichment strategy called CRISPR-Chromatin Affinity Purification with Mass Spectrometry (CRISPR-ChAP-MS) was used that provides for the proteomic characterization of a given locus. CRISPR-ChAP-MS was applied to the arsenic response locus and uncovered 40 nuclear-annotated proteins showing enrichment. Functional assays, identified the histone acetyltransferase activity of SAGA and the ATPase chromatin remodeling activity of SWI/SNF to be required for activation of the locus. Furthermore, SAGA and SWI/SNF were both found to specifically organize the chromatin structure at the arsenic response locus for activation of gene transcription. This study provides the first proteomic characterization of an arsenic response locus and key insight into the mechanism of transcriptional activation that is necessary for detoxification of arsenic from the cell.
2020-05-07 | PXD009902 | Pride
Project description:Arsenic (As) is a toxic environmental contaminant and potential human carcinogen. Chronic intake of arsenic-contaminated water leads to arsenicosis that is a major public health problem in many parts of the world, including India and Bangladesh. Thus, the early detection of arsenic toxicity will greatly benefit patients. However, the detection of arsenicosis needs to be done early before onset of severe symptoms in which case the tools used for detection have to be both sensitive and reliable. In this context, the present study investigated plasma proteome changes in arsenic-exposed Labeo rohita, with the aim of identifying biomarkers for arsenicosis. Changes in the plasma proteome were investigated using gel-based proteomics technology. Using quantitative image analysis of the 2D protein profiles, unique protein spots were identified from the plasma proteome by MALDI-TOF-TOF-MS. Unique proteins identified included Apolipoprotein-A1 (Apo-A1), α-2 macroglobulin-like protein (A2ML), and transferrin. Highly up-regulated protein spots identified in plasma from arsenic-exposed fish were liver-specific, including Apo-A1, and A2ML consistent with liver damage. It is proposed that a combination of these proteins could serve as useful biomarkers of hepatotoxicity and chronic liver disease due to arsenic exposure.
2017-05-11 | PXD003404 | Pride
Project description:Chronic arsenic exposure can lead to various health issues including cancer. There has been a growing concern about co-exposure to various prevalent lifestyle habits and their role in the enhancement of arsenic toxicity. Smokeless tobacco (SLT) products are extensively consumed in many South Asian countries, where their use frequently co-occurs with exposure to arsenic from contaminated groundwater. To decipher the oral epithelial cell responses to arsenic and SLT alone and in co-exposure, we performed multi-omics analyses of DNA methylome, transcriptomic reprogramming and genotoxic effects in controlled experimental settings. Chronic exposure studies revealed hypomethylation of genes involved in inflammation response and apoptosis, further corroborated by the upregulation of genes involved in these processes due to arsenic and the combined treatment in acute exposure setting. Next, to validate the omics results at the phenotypic level, we observed a dose dependent decrease in cell viability, induction of DNA damage, cell cycle changes, and an increase in apoptotic cells, with the most pronounced effects observed under arsenic and SLT co-exposure conditions. The observed DNA damage was likely the result of apoptosis induction, as chronic exposure experiments based on whole-exome sequencing did not reveal increased mutagenicity following the arsenic and/or SLT exposure. Our integrative omics study provides insights into both chronic and acute responses to arsenic and SLT co-exposure, with both types of responses converging on some of the same mechanisms. We identified large-scale epigenomic and transcriptomic reprograming associated with arsenic and SLT co-exposure, alongside genotoxic effects presumably manifesting as consequences of apoptosis induction. The findings point to a role of arsenic and SLT in altering key molecular responses, especially in the context of the co-exposure, and call for further studies in humans in the areas of exposure, to validate the observed mechanisms.
2024-12-04 | GSE269688 | GEO
Project description:Chronic arsenic exposure can lead to various health issues including cancer. There has been a growing concern about co-exposure to various prevalent lifestyle habits and their role in the enhancement of arsenic toxicity. Smokeless tobacco (SLT) products are extensively consumed in many South Asian countries, where their use frequently co-occurs with exposure to arsenic from contaminated groundwater. To decipher the oral epithelial cell responses to arsenic and SLT alone and in co-exposure, we performed multi-omics analyses of DNA methylome, transcriptomic reprogramming and genotoxic effects in controlled experimental settings. Chronic exposure studies revealed hypomethylation of genes involved in inflammation response and apoptosis, further corroborated by the upregulation of genes involved in these processes due to arsenic and the combined treatment in acute exposure setting. Next, to validate the omics results at the phenotypic level, we observed a dose dependent decrease in cell viability, induction of DNA damage, cell cycle changes, and an increase in apoptotic cells, with the most pronounced effects observed under arsenic and SLT co-exposure conditions. The observed DNA damage was likely the result of apoptosis induction, as chronic exposure experiments based on whole-exome sequencing did not reveal increased mutagenicity following the arsenic and/or SLT exposure. Our integrative omics study provides insights into both chronic and acute responses to arsenic and SLT co-exposure, with both types of responses converging on some of the same mechanisms. We identified large-scale epigenomic and transcriptomic reprograming associated with arsenic and SLT co-exposure, alongside genotoxic effects presumably manifesting as consequences of apoptosis induction. The findings point to a role of arsenic and SLT in altering key molecular responses, especially in the context of the co-exposure, and call for further studies in humans in the areas of exposure, to validate the observed mechanisms.
2024-12-04 | GSE269103 | GEO
Project description:Arsenic contaminated groundwater Raw sequence reads
| PRJNA291121 | ENA
Project description:Arsenic contaminated groundwater Raw sequence reads
| PRJNA481093 | ENA