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Links from GEO DataSets

Items: 7

1.
Full record GDS3670

Hypochlorous acid effect on macrophage cell line: dose response

Analysis of macrophage RAW 264.7 cells treated with up to 3.5 mM hypochlorous acid (HOCl). HOCl exposure can occur from chlorine gas inhalation or from endogenous sources of HOCl, such as respiratory burst by phagocytes. Results provide insight into the dose-dependent molecular response to HOCl.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 8 dose sets
Platform:
GPL1261
Series:
GSE15457
25 Samples
Download data: CEL
2.

Gene Expression Profiling of Cellular Dose-Response to Hypochlorous Acid (HOCl)

(Submitter supplied) Hypochlorous acid (HOCl) is a potent oxidant that is produced endogenously in mammalian tissue by phagocytes. Exogenous exposure to HOCl also can occur following inhalation of chlorine gas. HOCl has been implicated as a source of oxidative stress associated atherosclerosis and other diseases. The purpose of this study was to identify dose-dependent transitions in cellular response to hypochlorous acid (HOCl), with a focus on understanding how various cellular defense and stress dose-responses overlap.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3670
Platform:
GPL1261
25 Samples
Download data: CEL
Series
Accession:
GSE15457
ID:
200015457
3.

HOCL induced airway epithelial gene expression

(Submitter supplied) In inflammatory diseases of the airway, a high level (estimated to be as high as 8 mM) of HOCl can be generated through a reaction catalyzed by the leukocyte granule enzyme myeloperoxidase (MPO). HOCl, a potent oxidative agent, causes extensive tissue injury through its reaction with various cellular substances, including thiols, nucleotides, and amines. In addition to its physiological source, HOCl can also be generated by chlorine gas inhalation from an accident or a potential terrorist attack. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3363
Platform:
GPL571
32 Samples
Download data: CEL
Series
Accession:
GSE11630
ID:
200011630
4.
Full record GDS3363

Airway epithelial cells response to hypochlorous acid: time course

Temporal analysis of primary airway epithelial cells (AEC) treated with 0.4, 1 or 4mM hypochlorous acid (HOCl). HOCl is a potent oxidative agent that can be generated by neutrophils in inflammatory diseases of airways. Results provide insight into mechanisms underlying HOCl-induced toxicity in AECs.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 dose, 4 individual, 2 time sets
Platform:
GPL571
Series:
GSE11630
32 Samples
Download data: CEL
DataSet
Accession:
GDS3363
ID:
3363
5.

Response of Pseudomonas aeruginosa to the innate immune system-derived oxidants hypochlorous acid and hypothiocyanous acid

(Submitter supplied) Purpose: The aim of this study was to determine the transcriptional response of P. aeruginosa PA14 to HOCl and HOSCN stress, and determine genes dependent on RclR (PA14_07340) regulation. Methods: PA14 WT and ∆rclR exponential phase cultures were exposed to sub-lethal amounts of HOCl or HOSCN (2.2 or 0.8 mM, respectively), or untreated, and after 20 minutes of exposure, RNA was extracted and gene expression analysed by RNA-seq. more...
Organism:
Pseudomonas aeruginosa
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21297
12 Samples
Download data: XLSX
Series
Accession:
GSE124385
ID:
200124385
6.

RNA sequencing of Escherichia coli Nissle 1917 after HOCl stress

(Submitter supplied) RNA sequencing of Escherichia coli Nissle 1917 before and after HOCl treatment was perfomed to identify pathways that may be important in responding to oxidative stress caused by reachive chlorine species (RCS).
Organism:
Escherichia coli
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21222
9 Samples
Download data: XLSX
Series
Accession:
GSE144068
ID:
200144068
7.

Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription

(Submitter supplied) Nrf2 (NF-E2-related factor-2) transcription factor regulates oxidative/xenobiotic stress response and also represses inflammation. However, the mechanisms how Nrf2 alleviates inflammation are still unclear. Here, we demonstrate that Nrf2 interferes with lipopolysaccharide-induced transcriptional upregulation of proinflammatory cytokines, including IL-6 and IL-1β. ChIP-seq and ChIP-qPCR analyses revealed that Nrf2 binds to the proximity of these genes in macrophages and inhibits RNA Pol II recruitment. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL7202
12 Samples
Download data: TXT
Series
Accession:
GSE71263
ID:
200071263
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Supplemental Content

db=gds|term=|query=8|qty=5|blobid=MCID_67359da0909f1e7b1317f458|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
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