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Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from both wild-type and MAVS-/- mice

ABSTRACT: We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection Fully differentiated MTEC cells were infected with PR8 (moi: 0.3) or mock infected and RNA was collected at 24 hours post infection

ORGANISM(S): Mus musculus

SUBMITTER: Stefania Crotta

PROVIDER: E-GEOD-43709 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC)

Project description:We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection Fully differentiated MTEC cells were infected with PR8 (moi: 0.3) or mock infected and RNA was collected at 24 hours post infection

2013-08-30 | E-GEOD-43707 | biostudies-arrayexpress

Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from wild-type, IFNAR1-/-, IL28Ra-/- and IFNAR1-/- IL28Ra-/- double ko

2013-08-30 | E-GEOD-43708 | biostudies-arrayexpress

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-30 | E-GEOD-43710 | biostudies-arrayexpress

Environmental factors transmitted by aryl hydrocarbon receptor influence severity of psoriatic skin inflammation [Affymetrix]

Project description:Environmental stimuli are known to contribute to psoriasis pathogenesis and that of other autoimmune diseases, but the mechanism is unknown. Here we show that the aryl hydrocarbon receptor (AhR), a transcription factor that senses environmental stimuli, modulates pathology in psoriasis. AhR-activating ligands reduced inflammation in the lesional skin of psoriasis patients, whereas AhR antagonists upregulated inflammation. Similarly, AhR signaling via the endogenous FICZ ligand reduced the inflammatory response in the imiquimod-induced model of psoriasis and AhR deficient mice exhibited a substantial exacerbation of the disease, compared to AhR sufficient controls. Non-haematopoietic cells, in particular keratinocytes, were responsible for this hyper-inflammatory response, which involved increased reactivity to IL-1beta and upregulation of AP-1 family members of transcription factors. Thus, our data suggest a critical role for AhR in the regulation of inflammatory responses and open the possibility for novel therapeutic strategies in chronic inflammatory disorders. Total RNA obtained from skin explants taken from AhR heterozygous or knock-out mice treated pericutaneously with imiquimod for 0 and 2d.

2014-06-11 | E-GEOD-47607 | biostudies-arrayexpress

Environmental factors transmitted by aryl hydrocarbon receptor influence severity of psoriatic skin inflammation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-11 | E-GEOD-47965 | biostudies-arrayexpress

Expression data from early and late passages of OVDM1 cell line and the original metastatic tumor

Project description:OVDM1, a new ovarian cell line derived from a serous ovarian metastatic adenocarcinoma sample, was established by immortalization with SV40 large-T antigen and hTERT and then characterized Expression microarrays were used for molecular profiling of early and late passages of OVDM1 cell line, as well as the original metastatic tumor. Total RNA was extracted from early and late passages of OVDM1 and from the metastatic tumor for hybridization on Affymetrix microarrays

2016-06-01 | E-GEOD-70264 | biostudies-arrayexpress

Expression data from chemokine-deficient mus musculus subjected to traumatic brain injury (TBI)

Project description:We inflicted TBI to chemokine-deficient mouse lines in order to establish involvement of various signalling pathways that may be addressed therapeutically. Interacting chemokine pathways in brain regulate distinct inflammatory cells. Activated microglia are separate from invading phagocytes and dendritic cells. Findings show potential targets to interfere with specific inflammatory responses after brain injury. TBI was carried out in Ccl3-/- and Ccr2-/- mice, total RNA prepared from injured cerebral neocortex after three days. RNA samples were from uninjured Ccl3-/- and Ccr2-/- mice as reference for hybridization on Affymetrix microarrays.

2014-06-14 | E-GEOD-58483 | biostudies-arrayexpress

Genome-wide gene expression analysis in Thoc5- and CFIm68-depleted HeLa cells

Project description:We found that CFIm68, a mRNA cleavage and polyadenylation factor implicated for alternative polyadenylation site choice, was co-purified with Thoc5, a component of human THO/TREX. Microarray analysis using human HeLa cells reveals knockdown of Thoc5 affects the expression of a subset of non-heat shock genes. Notably, depletion of Thoc5 attenuated the expression of the mRNAs polyadenylated at distal, but not proximal, polyadenylation sites, which phenocopied the depletion of CFIm68. Two independent experiments using different siRNAs against Thoc5 (siThoc5-1and siThoc5-2) and CFIm68 (siCFIm68-1and siCFIm68-2) were performed. In both experiments, siDsRed was used as negative control.

2013-05-21 | E-GEOD-42327 | biostudies-arrayexpress

Identification and functional analysis of SHISA2 overexpressed in high-grade prostate cancer cells.

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2013-09-13 | E-GEOD-48833 | biostudies-arrayexpress

Expression data from mus musculus subjected to traumatic brain injury (TBI) for treatment with cyclophosphamide

Project description:We inflicted TBI to wildetype (wt) mice in order to establish whether the anti-inflammatory agent cyclophosphamide can be used therapeutically. Cyclophosphamide was found to regulate distinct inflammatory cells such as activated microglia separate from invading phagocytes and dendritic cells. Cyclophosphamide postinjury selectively reduces antigen-presenting dendritic cells. Findings show feasibility of drug development to interfere with brain inflammation. TBI was carried out in injured wt B6 mice for postinjury treatment with cyclophospamide i.p. using saline as a control substance for comparison with injured but untreated mice. Total RNA was prepared from injured cerebral neocortex after three days. RNA samples were also from uninjured wt mice as reference for hybridization on Affymetrix microarrays.

2014-06-14 | E-GEOD-58484 | biostudies-arrayexpress

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