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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiles of Ad-F7 transduced macrophages treated with anti-IFNAR2 antibody or control isotype (IgG)

ABSTRACT: Determine the role of interferons in the transcriptional profile of Ad-F7 transduced primary human macrophages using neutralizing antibody for the type I IFN receptor (IFNAR2). Primary human macrophage preparations were transduced with Ad-GFP or Ad-F7 and treated with control isotype (IgG) or neutralizing antibody for the type I IFN receptor (IFNAR2). RNA was collected 24 hours later and subjected to microarray analysis. Data represents the average of 5 donors.

ORGANISM(S): Homo sapiens

SUBMITTER: Eduardo Hernandez

PROVIDER: E-GEOD-12002 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.

Goubau Delphine D Romieu-Mourez Raphaëlle R Solis Mayra M Hernandez Eduardo E Mesplède Thibault T Lin Rongtuan R Leaman Douglas D Hiscott John J

European journal of immunology 20090201 2

The immunoregulatory transcriptional modulators - IFN-regulatory factor (IRF)-3 and IRF-7 - possess similar structural features but distinct gene-regulatory potentials. For example, adenovirus-mediated transduction of the constitutively active form of IRF-3 triggered cell death in primary human MPhi, whereas expression of active IRF-7 induced a strong anti-tumoral activity in vitro. To further characterize target genes involved in these distinct cellular responses, transcriptional profiles of ac ...[more]

PMID: 19152337

Similar Datasets

Transcriptional re-programming of primary human macrophages by IRF-3 and IRF-7

Project description:This SuperSeries is composed of the following subset Series: GSE11926: Transcriptional profiles of Ad-F3 and Ad-F7 transduced macrophages. GSE12002: Transcriptional profiles of Ad-F7 transduced macrophages in the presence of neutralizing antibody for the type I interferon receptor (IFNAR2) or control isotype (IgG). Refer to individual Series

2008-11-29 | E-GEOD-12120 | biostudies-arrayexpress

Transcriptional profiles of Ad-F3 and Ad-F7 transduced macrophages

Project description:To identify genes that may regulate distinct or overlapping functions of IRF-3 and IRF-7, primary human macrophage preparations were transduced with adenoviral vectors: Ad-GFP (control), Ad-F3 (expressing the active form of IRF-3, IRF-3 5D), or Ad-F7 (expressing the active form of IRF-7, IRF-7 D247-467) and evaluated by microarray analysis. RNA was collected 24 hours post-transduction with Ad-GFP, Ad-F3 and Ad-F7 and subjected to microarray analysis. Submited tables show the average of 7 donors.

2008-11-29 | E-GEOD-11926 | biostudies-arrayexpress

Transcriptional profiles of Ad-F7 transduced macrophages treated with anti-IFNAR2 antibody or control isotype (IgG)

Project description:Determine the role of interferons in the transcriptional profile of Ad-F7 transduced primary human macrophages using neutralizing antibody for the type I IFN receptor (IFNAR2).

2008-11-30 | GSE12002 | GEO

Project description:The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (?) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (?/?) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits type I interferon responses when targeted to the host endo-lysosomal system. While live Toxoplasma fails to induce type I interferon, heat-killed parasites do trigger this response, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that some parasite species, like Toxoplasma gondii, have evolved mechanisms to suppress this response. In vitro cultures of bone marrow-derived macrophages from WT or IFNAR2-/- mice were infected with either Toxoplasma gondii (VEG strain) or Neospora caninum (Nc2 strain) for 17 hours. RNA was collected from biological replicates for expression profiling by microarray. Uninfected controls for both WT and IFNAR2-/- were used as a reference.

2013-03-29 | E-GEOD-45632 | biostudies-arrayexpress

Homo sapiens

Project description:Transcriptional profiles of Ad-F7 transduced macrophages treated with anti-IFNAR2 antibody or control isotype (IgG)

| PRJNA114297 | ENA

Expression data from primary hepatocytes knocking down or overexpressing IRE1a

Project description:The ER-resident protein kinase/endoribonuclease IRE1 is activated through trans-autophosphorylation in response to protein folding overload in the ER lumen and maintains ER homeostasis by triggering a key branch of the unfolded protein response. Here we show that mammalian IRE1a in liver cells is also phosphorylated by a kinase other than itself in response to metabolic stimuli. Glucagon stimulated protein kinase PKA, which in turn phosphorylated IRE1a at Ser724, a highly conserved site within the kinase activation domain. Blocking Ser724 phosphorylation impaired the ability of IRE1a to augment the upregulation by glucagon signaling of the expression of gluconeogenic genes. Moreover, hepatic IRE1a was highly phosphorylated at Ser724 by PKA in mice with obesity, and silencing hepatic IRE1a markedly reduced hyperglycemia and glucose intolerance. Hence, these results suggest that IRE1a integrates signals from both the ER lumen and the cytoplasm in the liver and is coupled to the glucagon signaling in the regulation of glucose metabolism. We used DNA microarray to analyze the transcriptomic change upon IRE1a overexpression or IRE1a depletion in primary hepatocytes, to study the changes related to IRE1a Primary hepatocytes were infected with the desired adenoviruses (Ad-EGFP, Ad-WT, Ad-S724A, Ad-shCON, Ad-shIRE1a#2) or treated with glucagon. Total cellular RNA was isolated with TRIzol (Invitrogen) and subjected to analysis by Affymetrix Mouse Genome 430 2.0 Arrays. Three experiments were independently conducted.

2011-08-30 | E-GEOD-31638 | biostudies-arrayexpress

Transcriptional profiles of Ad-F3 and Ad-F7 transduced macrophages

2008-11-30 | GSE11926 | GEO

Homo sapiens

Project description:Transcriptional profiles of Ad-F3 and Ad-F7 transduced macrophages

| PRJNA113827 | ENA

Regulation of HSF1-mediated transcriptional programs by PGC-1alpha

Project description:We examined global gene expression patterns in response to PGC-1 expression in cells derived from liver or muscle. As our study revealed regulation of HSF1 by PGC-1alpha, in some experiments we knocked-down HSF1 using siRNAs in addition to inducing PGC-1alpha expression. Cells were grown in 24-well plates and adenoviruses encoding either GFP ("Ad-GFP"), PGC-1alpha ("Ad-PGC-1alpha") or PGC-1beta ("Ad-PGC-1beta") were directly added to the culture medium. For experiments involving siRNA transfections, cells were transfected with the indicated siRNAs 48hr prior to infection with adenoviruses encoding either GFP ("Ad-GFP") or PGC-1alpha ("Ad-PGC-1alpha").

2015-09-19 | E-GEOD-51498 | biostudies-arrayexpress

Structural basis of a novel Interferon b signaling axis mediated via the ifnar1 receptor

Project description:Type I interferons (IFNs) are a family of cytokines that play an important role in regulating immune responses to pathogens and tumors and are used therapeutically. All IFNs are considered to signal via the heterodimeric IFNAR1-IFNAR2 complex, yet some subtypes such as IFN? can exhibit distinct functional properties, although the molecular basis of this is unclear. Here we demonstrate IFN uniquely and specifically ligates to IFNAR1 in an IFNAR2-independent manner and provide the structural basis of the IFNAR1-IFN interaction. We show that the IFNAR1-IFN complex transduces signals to modulate the expression of a set of genes independently of IFNAR2. Moreover, we show the in vivo importance of the IFNAR1-IFN signaling axis in a murine model of LPS-induced septic shock. Thus, we provide a molecular basis for understanding specific functions of IFN?. Interferon b induced gene expression in peritoneal exudate cells was measured 3hr post intra-peritoneal injection of 10,000IU/ml of interferon beta or saline into wildtype and Ifnar2-/- mice. Three independant experiments were performed for each treatment in both genotypes using different mice for each sample.

2013-07-13 | E-GEOD-48827 | biostudies-arrayexpress

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