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Expression Data from siRae1 and siNT infected with VSV or mock infected

ABSTRACT: To test the effect of silencing Rae1 on expression on RNA polymerase II transcripts, host mRNAs were analysed by cDNA microarrays. We hypothesized that if silencing Rae1 expression increases cellular resistance to inhibition of transcription in VSV infected cells, mRNA characteristic of host antiviral response would be increased than compared to cells transfected with control siRNA. HeLa cells transfected with siRNA targeted against Rae1 (siRae1) or against non-targeting siRNA (siNT). The sequence of nontargeting (NT) siRNA is scrambled and does not match any sequence on the human genome. Transfected cells were either infected with VSV or mock infected. Six hours later RNA was extracted from the cells. Two separate experiments of such were analyzed by microarrays

ORGANISM(S): Homo sapiens

SUBMITTER: Jeff Chou

PROVIDER: E-GEOD-38866 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression Data from siRae1 and siNT infected with VSV or mock infected

Project description:To test the effect of silencing Rae1 on expression on RNA polymerase II transcripts, host mRNAs were analysed by cDNA microarrays. We hypothesized that if silencing Rae1 expression increases cellular resistance to inhibition of transcription in VSV infected cells, mRNA characteristic of host antiviral response would be increased than compared to cells transfected with control siRNA.

2012-06-29 | GSE38866 | GEO

SIK2-dependent Phosphoproteome and Interactome upon Salmonella infection

Project description:HeLa cells transfected with non-targeting control- and anti-SIK2 siRNA were left uninfected or infected with Salmonella and lysed 30 min pi. Following tryptic-digest peptides were labeled using TMT-pro 16-plex and phosphopeptides enriched. The endogenously tagged SIK2-HA IP workflow. Hela wild type or endogenous SIK2-HA-tagged HeLa cells were left uninfected or infected with Salmonella and lysed 1 h post-infection, followed by HA-IP, Tryptic digest, TMT-labeling and LC-MS/MS analysis.

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Gene expression comparison between two human cancer cell Lines: Oral squamous cell carcinoma SASL1m and adenoid cystic carcinoma ACC2

Project description:SASL1 is highly metastatic to lymph nodes. ACC2 is not metastatic. We compared gene expression on cultured cells to identify genes associated to metastatic spread patterns. SASL1m cells and ACC2 cells were cultured to confluence in 10 100mm dishes (5 per cell type). Total RNA was extracted (ISOGEN, Nippongene, Japan), purified by centrifugation, pooled and checked for quality (Eukaryote Total RNA Series II, Agilent, Sta Clara, USA) . Two samples of 2ɥg of Total RNA from SASL1m and ACC2 cells were labeled with biotin (3'IVT Labeling Kit, Affymetrix, USA) and hybridized (GeneAtlas Hybridization, Wash, and Stain Kit for 3' IVT Arrays, Affymetrix). The Microarray platform used was Affymetrix HG U219 Array Strip. The arrays were scanned in a GeneAtlas scanner controlled by GeneAtlas Software (Affymetrix, Sta. Clara, USA). No replicates were made. Genes were later filtered according to expression fold change (GeneSpring GX Software, Agilent, Sta Clara USA) and later organized in hypothetical networks (Ingenuity Pathway and Analysis Software, Ingenuity Systems, Redwood, USA). No control or reference samples were included. The expression of genes of interest was confirmed with qrt-PCR in the samples studied and four additional samples from cell cultures (Lightcycler, Roche, Switzerland).

2011-10-24 | E-GEOD-33171 | biostudies-arrayexpress

Deregulation of genes in SH-SY5Y treated with supernatant from U-937-HIV-1 infected cells

Project description:It is well known that HIV-1 does not infect neurons, however neurons are the most affected cells by the virus. Several studies linked the deregulation of neuronal transcriptional machinery to single HIV proteins, however the impact of the all the viral proteins on neurons remain unknown. In here we infected U-937 cells with JR-FL strain of HIV-1. 21 days later, the supernatants were collected and subjected to p24ELISA to measure the level of the virus. Supernatant was then added to SH-SY5Y cells in culture for 24hrs. The cells were then collected, RNA isolated and subjected to gene array analysis. Human neuronal cell line, SH-SY5Y were chosen to examine the impact of HIV-1 supernatant prepared from U-937 infected cells on gene expression in neuronal cells.

2012-12-07 | E-GEOD-42615 | biostudies-arrayexpress

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders [differentiated SH-5Y cells]

Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Vpr protein on gene expression

2013-01-17 | E-GEOD-43535 | biostudies-arrayexpress

Profiling study of B cells from lymph nodes in miR-146a over-expression transgenic mice

Project description:B cells were isolated from wild type and miR-146a transgenic mice, and analyzed using microarray assay.WT1 and WT2 were samples repeats, so were TG1 and TG2 . Each probe ID of a mouse transcript was ranked by fold change from up to down-regulated comparing to WT control. Sylamer miRNA seed enrichment analysis was performed with Markov correction as described (Nature Method 2008). WT vs. TG.

2012-08-07 | E-GEOD-39779 | biostudies-arrayexpress

UV-RIP experiments of ZNFX1 in VSV infected A549 cells

Project description:UV-RIP-seq was used to identify VSV-RNA associated with endogenous ZNFX1 in VSV infected A459 cells.

2019-08-30 | GSE132977 | GEO

Analysis of global gene expression profiles of hPAF1 deficient A549 cells during infection with H1N1 influenza A virus or vesicular stomatitis virus (VSV)

Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 targets the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. More importantly,in the following data sets, we show that hPAF1 plays a crucial role in the antiviral response. Loss of hPAF1C reduces antiviral gene expression and reduces inducible transcription of target genes after stimulation with viral RNA analogue poly(I:C), vesicular stomatitis virus (VSV), exogenous recombinant IFN(beta) and influenza virus (H1N1). This study underscores the importance of hPAF1C in controlling inducible antiviral gene expression. Untreated (no siRNA), control siRNA-treated and hPAF1 siRNA-treated A549 cells were stimulated with A/Puerto Rico/8/1934 influenza virus (H1N1) or vesicular stomatitis virus (VSV). Total RNA was isolated with the Qiagen RNeasy mini kit. 200ng of total RNA per sample was used to prepare biotin-labeled RNA using MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems) and hybridized to HumanHT-12 v4 Expression BeadChips (Illumina). Data analysis was performed using the GeneSpring GX11.0 software (Agilent Technologies). 3 biological replicates per condition

2012-02-15 | E-GEOD-35266 | biostudies-arrayexpress

Genome-wide transcriptional profiling of Legionella Pneumophila-infected A549 cells transfected with siRNA against TNFAIP2

Project description:In this study we transfected A549 cells with siRNA against TNFAIP2, infected them with L. pneumophila and performed transcriptional profiling. We found enrichment of genes in pro-inflammatory pathways by Pathway Over-respresentation analysis upon infection. There was no significant change in gene expression that we could attribute specifically to the knockdown of TNFAIP2. Examination of the transcriptional response of A549 cells to Legionella infection with concomitant TNFAIP2 knockdown

2016-04-13 | E-GEOD-80214 | biostudies-arrayexpress

HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs [differentiated SH-5Y cells]

Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Tat protein on gene expression

2013-01-17 | E-GEOD-43534 | biostudies-arrayexpress

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