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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

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

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

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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;

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