Similar Datasets
Project description:Arsenic Toxicity in the Drosophila Brain at Single Cell Resolution
| PRJNA1231228 | ENA
Project description:Genetic analysis of women from the Andes Mountains that are exposed to arsenic in drinking water.
| EGAS00001001168 | EGA
Project description:This SuperSeries is composed of the following subset Series: GSE16769: Male and female Fundulus exposed to 172ppb arsenic, and their parentally exposed offspring GSE16770: Male and female Fundulus exposed to 575ppb arsenic, and their parentally exposed offspring GSE16771: Male Fundulus exposed to 1,720ppb arsenic, and their parentally exposed offspring Refer to individual Series
2009-06-24 | E-GEOD-16772 | biostudies-arrayexpress
Project description:Talemi2014 - Arsenic toxicity and
detoxification mechanisms in yeast
The model implements arsenite (AsIII)
transport regulation, its distribution within main cellular AsIII
pools and detoxification. The intracellular As pools considered are
free AsIII (AsIIIin), protein-bound AsIII (AsIIIprot), glutathione
conjugated AsIII (AsGS3) and vacuolar sequestered AsIII (vAsGS3).
This model is described in the article:
Mathematical modelling of
arsenic transport, distribution and detoxification processes in
yeast.
Talemi SR, Jacobson T, Garla V,
Navarrete C, Wagner A, Tamás MJ, Schaber J.
Mol. Microbiol. 2014 Jun; 92(6):
1343-1356
Abstract:
Arsenic has a dual role as causative and curative agent of
human disease. Therefore, there is considerable interest in
elucidating arsenic toxicity and detoxification mechanisms. By
an ensemble modelling approach, we identified a best
parsimonious mathematical model which recapitulates and
predicts intracellular arsenic dynamics for different
conditions and mutants, thereby providing novel insights into
arsenic toxicity and detoxification mechanisms in yeast, which
could partly be confirmed experimentally by dedicated
experiments. Specifically, our analyses suggest that: (i)
arsenic is mainly protein-bound during short-term (acute)
exposure, whereas glutathione-conjugated arsenic dominates
during long-term (chronic) exposure, (ii) arsenic is not stably
retained, but can leave the vacuole via an export mechanism,
and (iii) Fps1 is controlled by Hog1-dependent and
Hog1-independent mechanisms during arsenite stress. Our results
challenge glutathione depletion as a key mechanism for arsenic
toxicity and instead suggest that (iv) increased glutathione
biosynthesis protects the proteome against the damaging effects
of arsenic and that (v) widespread protein inactivation
contributes to the toxicity of this metalloid. Our work in
yeast may prove useful to elucidate similar mechanisms in
higher eukaryotes and have implications for the use of arsenic
in medical therapy.
This model is hosted on
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and identified by:
BIOMD0000000547.
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To the extent possible under law, all copyright and related or
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2024-09-02 | BIOMD0000000547 | BioModels
Project description:Human bronchial epithelial cell BEAS-2B cells were continuously exposed to a vehicel control (DMSO), arsenic (NaAsO2, 1 uM), BaP (2.5 um) alone or arsenic plus BaP for 30 weeks. At the end of exposure, cells were collected and total RNA was extracted for microarray analysis.
2022-05-18 | GSE149605 | GEO
Project description:The present study used microarray expression profiling to determine the effects of embryonic arsenic exposure. Fertilized killifish (Fundulus heteroclitus) eggs were exposed to 0, 5, 15, or 25ppm arsenic as sodium arsenite. To examine differentially expressed genes, the microarrays were probed using RNA obtained from the control and 25ppm-exposed killifish just after hatching. No differences were noted in survival or hatching success between any of the groups. After analysis, a set of 332 genes was found to accurately distinguish between the control and 25ppm exposure groups. Expression of several of the genes (CDBP1, Arts1, FetB, and Fbp7) was quantified by qPCR in the lower exposure groups and at earlier time points to examine temporal and dose-responsive expression patterns. These results will enable us to better understand how arsenic impacts development. Killifish eggs were fertilized, divided into petri dishes containing 40 eggs (n=10 replicate petri dishes), and cultured until hatch in 0 or 25 ppm arsenic as sodium arsenite. Four to five hatchlings within each petri dish were pooled to obtain RNA. A total of 20 arrays were probed, 10 with RNA from control fish and 10 with RNA from the arsenic-exposed fish.
2011-07-31 | E-GEOD-29976 | biostudies-arrayexpress
Project description:The present study used microarray expression profiling to determine the effects of embryonic arsenic exposure. Fertilized killifish (Fundulus heteroclitus) eggs were exposed to 0, 5, 15, or 25ppm arsenic as sodium arsenite. To examine differentially expressed genes, the microarrays were probed using RNA obtained from the control and 25ppm-exposed killifish just after hatching. No differences were noted in survival or hatching success between any of the groups. After analysis, a set of 332 genes was found to accurately distinguish between the control and 25ppm exposure groups. Expression of several of the genes (CDBP1, Arts1, FetB, and Fbp7) was quantified by qPCR in the lower exposure groups and at earlier time points to examine temporal and dose-responsive expression patterns. These results will enable us to better understand how arsenic impacts development.
2011-08-01 | GSE29976 | GEO
Project description:Total RNA was purified from keratinocytes isolated from FFPE arsenic-induced skin lesion samples collected from individuals exposed to high concentrations of arsenic exceeding 50 ppb in drinking water in Murshidibad district of West Bengal, India.
2018-06-01 | GSE102892 | GEO
Project description:In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 60 mg/L (192?M) arsenic [As(V)] for 8-96 h, to identify global transcriptional programs and biological networks involved in arsenic-induced adaptive responses in vivo. We identified temporal differentially-expressed gene sets which we have grouped into early, late and all-time arsenic-responsive gene sets. Keywords: compound treatment design
2006-08-02 | GSE3048 | GEO