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Expression data from edema toxin treated primary hepatocytes from 1–3-day-old neonatal A/J mice

ABSTRACT: Expression data from edema toxin treated primary hepatocytes from 1–3-day-old neonatal A/J mice

PROVIDER: PRJNA476255 | ENA |

REPOSITORIES: ENA

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Expression data from edema toxin treated primary hepatocytes from 1–3-day-old neonatal A/J mice

Project description:The activity of known anthrax toxins is insufficient to account the effects on functions of hepatocytes. In vivo and in vitro studies showed that Anthrax edema toxin (EdTx) induce lethal liver and heart damage We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process.

2018-06-16 | GSE115844 | GEO

Edema Toxin-treated Macrophage Study

Project description:Edema toxin (EdTx), which is a combination of edema factor and a binding moiety (protective antigen), is produced by Bacillus anthracis, the etiological agent of anthrax. EdTx is an adenylyl cyclase enzyme that converts adenosine triphosphate to adenosine-3’,5’-monophosphate, resulting in interstitial edema seen in anthrax patients. We used GeneChip analysis to examine global transcriptional profiles of EdTx-treated RAW 264.7 murine macrophage-like cells at 3 and 6 hr. Keywords: Toxin response

2006-10-24 | GSE4712 | GEO

Expression data from anthrax lethal toxin treated primary cardiomyocytes from 1-3-day-old neonatal Balb/c mice

Project description:The activity of known anthrax lethal toxin is insufficient to account the effects on functions of cardiomyocytes. In vivo and in vitro studies showed that Anthrax lethal toxin (LeTx) induce heart damage We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process.

2018-07-07 | GSE116755 | GEO

Expression data from anthrax lethal toxin treated primary cardiomyocytes from 1-3-day-old neonatal Balb/c mice

Project description:Expression data from anthrax lethal toxin treated primary cardiomyocytes from 1-3-day-old neonatal Balb/c mice

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Plant toxin treatment of neonatal mouse cholangiocytes

Project description:Plant toxin treatment of neonatal mouse cholangiocytes

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Transcription profiling of rat neonatal ventricular cardiac mycocytes exposed to endothelin-1 and C3 toxin

Project description:Effects of C3 toxin on RNA profiles in neonatal rat ventricular cardiac myocytes exposed to endothelin-1 (1 h)

2010-05-25 | E-MEXP-1977 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow derived macrophages (BMDM) treated with anthrax edema toxin (ET)

Project description:Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Experiment Overall Design: BMDM were treated with 1 mg/ml of ET and the RNAs were purified at 0, 2, and 4h after toxin treatment.

2008-06-16 | E-GEOD-9184 | biostudies-arrayexpress

Expression profile from anthrax edema toxin (ET) treated murine bone marrow derived macrophages (BMDM)

2007-09-28 | GSE9184 | GEO

HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT) Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment.

2009-08-25 | GSE17777 | GEO

Transcription profiling of human HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator

Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT); Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.

2009-09-13 | E-GEOD-17777 | biostudies-arrayexpress

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