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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Eduardo Hernandez

PROVIDER: E-GEOD-12120 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

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

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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). 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.

2008-11-29 | E-GEOD-12002 | 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

Transcription profiling of sugarcane mosaic virus (SCMV) resistance in maize

Project description:The molecular mechanisms underlying the development and progression of sugarcane mosaic virus (SCMV) infection in maize are poorly understood. A transcript profiling study based on maize unigene-microarrays was conducted to identify genes associated with SCMV resistance in the near isogenic line (NIL) pair F7+ (SCMV resistant) and F7 (susceptible). Four comparisons were conducted, which is addressing constitutive genetic discrepancy (Non-infected F7 vs. Non-infected F7+), inducible genetic discrepancy (Infected F7 vs. Infected F7+), compatible reaction (Non-infected F7 vs. Infected F7), and incompatible reaction (Non-infected F7+ vs. Infected F7+).

2005-01-21 | E-MEXP-253 | biostudies-arrayexpress

Dynamic epigenetic enhancer signatures are predictive for key transcriptional regulators associated with cellular differentiation states

Project description:Cellular differentiation is orchestrated by lineage-specific transcription factors and associates with cell type-specific epigenetic signatures. Here, we utilized stage-specific, epigenetic "fingerprints" to deduce key transcriptional regulators of a cellular differentiation process. In the model of human macrophage differentiation, we globally mapped the distribution of epigenetic enhancer marks (histone H3 lysine 4 monomethylation, histone H3 lysine 27 acetylation, and the histone variant H2AZ) and show that cell type-specific epigenetic "fingerprints" correlate with specific, de novo derived motif signatures at all differentiation stages studied (hematopoietic progenitor cell, monocyte, macrophage). We validated the novel, de novo derived, macrophage-specific enhancer signature which included ETS, CEBP, bZIP, EGR, E-Box and NFkB motifs by ChIP-sequencing for a subset of motif corresponding transcription factors (PU.1, C/EBPbeta, and EGR2) which confirmed their predicted association with differentiation-associated epigenetic changes. This study highlights the power of genome-wide epigenetic profiling studies to reveal novel functional insights. It describes the dynamic enhancer landscape of human macrophage differentiation and provides a unique resource for macrophage biologists. ChIP-seq of 3 histone marks and 3 transcription factors in human blood monocytes and macrophages

2012-05-02 | E-GEOD-31621 | biostudies-arrayexpress

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

small RNA Next Generation Sequencing of human primary macrophages treated with staurosporine

Project description:Human primary macrophages were treated with 1 µM staurosporine (STS) and profiled for small RNAs. Human primary macrophages were treated with 1 µM staurosporine (STS) for 0, 4 and 6h.

2015-09-16 | E-GEOD-47608 | biostudies-arrayexpress

microRNA profiling of human monocytes and monocyte-derived macrophages

Project description:microRNA profiling data includes biological replicates of primary monocytes and macrophages from three human donors Dye swap hybridization arrays were performed for total RNA isolated from fresh monocytes and 7-day monocyte-derived macrophages from each of three human donors

2013-05-10 | E-GEOD-39905 | biostudies-arrayexpress

1GDAP1 loss of function inhibits the mitochondrial pyruvate dehydrogenase complex by altering the actin cytoskeleton

Project description:Charcot-Marie-Tooth (CMT) disease 4A is an autosomal-recessive polyneuropathy caused by mutations of ganglioside-induced differentiation-associated protein 1 (GDAP1), a putative glutathione transferase, which affects mitochondrial shape and alters cellular Ca2+homeostasis. Here, we identify the underlying mechanism. We found that patient-derived motoneurons and GDAP1knockdown SH-SY5Y cells display two phenotypes: more tubular mitochondria and a metabolismcharacterized by glutamine dependence and fewer cytosoliclipid droplets. GDAP1 interacts with the actin-depolymerizing protein Cofilin-1 in a redox-dependent manner, suggesting a role for actin signaling. Consistently, GDAP1 loss causes less F-actin close to mitochondria, which restricts mitochondrial localization of the fission factor dynamin-related protein 1, instigating tubularity. Changes in the actin cytoskeleton also disrupt mitochondria-ER contact sites. This results in lower mitochondrial Ca2+levels and inhibition of the pyruvate dehydrogenase complex,explaining the metabolic changes upon GDAP1 loss of function. Together, these findings reconcile GDAP1-associated phenotypes and implicate disrupted actin signaling in CMT4A pathophysiology.

2022-08-12 | PXD024555 | Pride

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

2013-03-29 | E-GEOD-45634 | biostudies-arrayexpress

Transcription profiling of human macrophages from Crohns disease patients or healthy control individuals, either unstimulated or stimulated with heat killed E. coli;

Project description:Comparison of gene expression in macrophages from Crohn's disease patients or healthy control individuals, either unstimulated or stimulated with heat killed E. coli

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