Ontology highlight
ABSTRACT:
PROVIDER: PRJNA510150 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8324600.fastq.gz | Fastqsanger.gz | |||
| SRR8324601.fastq.gz | Fastqsanger.gz | |||
| SRR8324602.fastq.gz | Fastqsanger.gz | |||
| SRR8324603.fastq.gz | Fastqsanger.gz | |||
| SRR8324604.fastq.gz | Fastqsanger.gz |
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Project description:Microarray data was used to assess ATF4-dependent gene expression and signaling pathways induced by arsenite in mouse cortical neurons. Pathway enrichment analysis of differentially expressed genes revealed several ATF4-dependent signaling pathways induced by arsenite treatment in mouse neurons.
2026-07-01 | GSE336776 | GEO
Project description:miRNA Array was used to detect the expression level of miRNAs in human bronchial epithelial (HBE) cells that were transformed by a low-level arsenite exposure for 13 weeks. The transformed cells exhibited malignant phenotypes manifested by increased levels of cell proliferation, cell migration and high level of cell survival. Subsequently, 191 differentially expressed miRNAs are identified to be associated with arsenite-induced malignant transformation by employing miRNA Array. Among them, six miRNAs were chosen to validate their expression levels with qPCR and 17 miRNAs were further explored their target genes and the network. Three databases, TargetMiner, miRDB and TarBase, were used to predict the target genes of miRNAs and a total of 954 common genes were identified. Results of Gene Ontology (GO) analyses showed that these target genes were involved in diverse terms of GO categories, such as positive regulation of macroautophagy, epithelial cell maturation and synaptic vesicle clustering and so on. Moreover, results of KEGG pathway analyses demonstrated that most of these target genes were enriched in various cancer-related pathways including non-small cell lung cancer, Wnt signaling pathway, cell cycle, p53 signaling pathway and so forth. The miRNA-gene regulatory network, which was constructed by cytoscape software with miRNAs and their target genes, showed that the target genes were mainly regulated by miR-15b-5p, miR-106b-5p and miR-320d. Although more experimental verification is still needed to prove these predictions, our results may provide new insights into miRNA-mediated mechanisms underlying arsenite-induced malignant transformation.
2018-07-07 | GSE100753 | GEO
Project description:Background: Previously, we showed that gestational arsenite (As) exposure of F0 females increases hepatic tumors in the F2 males in C3H mice. However, the mechanisms have not yet been clarified. Methods: We detected genome wide site-specific DNA methylation by using reduced representative bisulfite sequence (RRBS) method. We used the data uploaded here and those with GSE Series accession number GSE111420 (CCN and CCTt) to detect differential methyrated cytosines between control groups and arsenite groups. Results: We clarified that DNA methylation of Tmem54 and Cd74 around TSS were downregulated and their gene expressions were accordingly upregulated in the liver tumor tissues of F2 males of arsenite group. Conclusions: Our study proposes novel DNA methylation dependent pathways which increase liver tumors in the F2 males of arsenite group.
2019-08-20 | GSE123749 | GEO
Project description:Arsenite is mainly used as insecticides, antiseptic and herbicides. It enters the food chain through soil contamination, and then impedes human health, including of reproductive systems. Early embryos, as the initial stage of mammalian life, are very sensitive to the environmental toxins and pollutants. However, whether and how arsenite disturbs the early embryo development remains unknown. Here, we used mouse early embryo as a model and found that arsenite exposure did not induce reactive oxygen species production, DNA damage and apoptosis in early mouse embryos. However, arsenite exposure made embryonic development arrest at the 2-cell stage by altering their gene expression patterns. The transcriptional profile in the arrested embryos showed abnormal maternal-to-zygote transition (MZT). More importantly, arsenite exposure attenuated H3K27ac modification enrichment at the promoter region of Brg1 (a key gene for MZT), which inhibited its transcription, and further affected MZT and early embryonic development. Taken together, these results suggest that arsenite exposure affects MZT by reducing the enrichment of H3K27ac on the embryonic genome, and ultimately induces early embryonic development arrest at the 2-cell stage.
2026-01-01 | GSE222534 | GEO
Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation. A total of eight (8) samples with two biological replicates under four separate conditions: wild-type treated with deionized H2O for 36 days (NT); chronic low-dose arsenic exposure of 1 uM of sodium arsenite (iAs-T) for 36 days; chronic arsenic exposure of 1 uM of sodium arsenite for 26 days followed by removal of sodium arsenite for 10 days, measured at day 36 (iAs-Rev); and chronic arsenic exposure of 1 uM of sodium arsenite for 26 days, followed by removal of sodium arsenite exposure for 10 days, followed by 1 uM of chronic sodium arsenite exposure for 10 days (measured at day 46) (iAs-Rev-T).
2015-05-05 | E-GEOD-60760 | biostudies-arrayexpress
Project description:Under stress conditions, cells reprogram their molecular machineries to mitigate damage and promote survival. Ubiquitin signaling is globally increased during oxidative stress, controlling protein fate and supporting stress defenses at several subcellular compartments. However, the rules driving subcellular ubiquitin localization to promote these concerted response mechanisms remain understudied. Here, we show that K63-linked ubiquitin chains, known to promote proteasome-independent pathways, accumulate primarily in non-cytosolic compartments during oxidative stress induced by sodium arsenite in mammalian cells. Subcellular ubiquitin proteomic analyses of non-cytosolic compartments revealed thousands of proteins ubiquitinated during oxidative stress and involved in pathways related to immune signaling and translation control. Moreover, subcellular proteome analyses also revealed proteins that are recruited to non-cytosolic compartments under stress, including a significant enrichment of helper ubiquitin-binding adaptors of the ATPase VCP that processes ubiquitinated substrates for downstream signaling. We further show that VCP recruitment to non-cytosolic compartments under arsenite stress occurs in a ubiquitin-dependent manner mediated by its adaptor NPLOC4. Additionally, we show that VCP and NPLOC4 activities are critical to sustain low levels of non-cytosolic K63-linked ubiquitin chains, supporting a cyclical model of ubiquitin conjugation and removal that is disrupted by cellular exposure to reactive oxygen species. This work deepens our understanding of the role of localized ubiquitin and VCP signaling in the basic mechanisms of stress response and highlights new pathways and molecular players that are essential to reshape the composition and function of the human subcellular proteome under dynamic environments.
2024-06-04 | MSV000094932 | MassIVE
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. Worms were exposed to 100nM Arsenite 48h after L4. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2021-10-19 | GSE110845 | GEO
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls 4 samples: 2 mRNA profiles of C.elegans 48h after L4 exposed to Arsenite; 2 mRNA profiles of C.elegans 48h after L4 as controls (H20). The N2 wild type (var. Bristol) strain was used.
2013-04-23 | E-GEOD-46257 | biostudies-arrayexpress
Project description:Growth arrest and DNA damage induced protein (GADD34) is a regulator of protein phosphatase 1 and promotes eIF2α dephosphorylation under conditions of various stress. eIF2α phosphorylation at Ser 51 is a key nodule controlling the general rate of protein synthesis and activation of integrated stress response pathways. In GADD34 knockout conditions, dysregulated eIF2α phosphorylation is likely to produce abnormalities in the integrated stres response. GADD34 can be induced by many different stresses but oxidative stress by arsenite produced highest GADD34 levels in various cell lines tested. We aim to evaluate early gene expression changes on arsenite treatment and examine if GADD34 influences the profile of genes induced by oxidative stress. Using microarrays, we investigated the impact of GADD34 knockout under conditions of oxidative stress induced by arsenite in mouse embryonic fibroblasts.
2017-08-27 | GSE60868 | GEO
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2013-04-23 | GSE46257 | GEO