Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA281473 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Agilent SurePrint G3 Human V2 GE 8×60K microarray-BEAS-2B cells treatment with NiCl2
| PRJNA281474 | ENA
Project description:Human bronchial lung cells (BEAS-2B) were treated for 6 weeks with low doses (0.5 µg/mL) of Ni and NiO nanoparticles and NiCl2. At the end of the exposure control and treated samples were submitted for RNA-Seq analysis (Hiseq2500). The overall goal of this experiment was to gain an in-depth understanding of the transcriptomic changes induced by low-dose, long-term exposure of human lung cells to Ni and NiO nanoparticles as well as to NiCl2 and to generate hypotheses related to their mechanisms of toxicity.
2020-04-19 | E-MTAB-8903 | biostudies-arrayexpress
Project description:We report the differential expression of circRNAs between T-BEAS-2B cells (cadmium-transformed BEAS-2B cells) and C-BEAS-2B cells (passage-matched control BEAS-2B cells) by high-throughput sequencing. T-BEAS-2B cells are BEAS-2B cells transformed by cadmium at 2.0 μM for twenty weeks, and C-BEAS-2B cells are their passage-matched control. RNAs were sequenced on Illumina HiSeq Xten platform in triplicates, and expressions of circRNAs were calculated by TPM (transcripts per kilobase of exon model per million mapped reads). Clean data per sample exceeds 10 GB. We find 235 significantly up-regulated circRNAs and 271 significantly down-regulated circRNAs in T-BEAS-2B cells relative to C-BEAS-2B cells. Our work provides clues and evidence for exploring the mechanism of circRNAs in cadmium carcinogenesis.
2024-01-26 | GSE165549 | GEO
Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).
2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress
Project description:Alterations in chromatin modifications, including DNA methylation and histone modification patterns, have been characterized under exposure of several environmental pollutants, including nickel. As with other carcinogenic metals, the mutagenic potential of nickel compounds is low and is not well correlated with its carcinogenic effects. Nickel exposure, however, is associated with alterations in chromatin modifications and related transcriptional programs, suggesting an alternative pathway whereby nickel exposure can lead to disease. To investigate the extent to which nickel exposure disrupts chromatin patterns, we profiled several histone modifications, including H3K4me3, H3K9ac, H3K27me3 and H3K9me2 as well as the insulator binding protein CTCF and the transcriptomes of control BEAS-2B cells and cells treated with nickel for 72 hours. Our results show significant alterations of the repressive histone modification H3K9me2 in nickel-exposed cells with spreading of H3K9me2 into new domains associated with gene silencing. We furthermore show that local regions of active chromatin can protect genes from nickel-induced H3K9me2 spreading. Interestingly, we show that nickel exposure selectively disrupts weaker CTCF sites, leading to spreading of H3K9me2 at these regions. These results have major implications in the understanding of how environmental carcinogens can affect chromatin dynamics and the consequences of chromatin domain disruption in disease progression. Treat BEAS-2B cells with NiCl2 for 72 hours and compare histone modification, CTCF binding to control BEAS-2B cells to see how they regulated gene expression by RNA-seq
2014-09-26 | E-GEOD-56051 | biostudies-arrayexpress
Project description:Effects of NiCl2 on gene and miRNA expression in BEAS-2B cells
| PRJNA281468 | ENA
Project description:BEAS-2B cells transfected with Dermatophagoides farinae miRNAs
| PRJNA1023698 | ENA
Project description:Illumina microarray experiment on BEAS-2B cells. Cells were seeded 24 h before TNF-a/IL-4 (50 ng/ml) treatment that lasted for 18 h. Cytoplasmic RNA of both normal and activated BEAS-2B cells were collected for microarray. Cells were seeded 24 h before TNF-a/IL-4 (50 ng/ml) treatment that lasted for 18 h.
2008-10-14 | GSE13119 | GEO