Background
STOX1 overexpression in choriocarcinoma cells mimics transcriptional alterations observed in preeclamptic placentas.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dynamic O-GlcNAc cycling at promoters of Caenorhabditis elegans genes regulating longevity, stress, and immunity.
No sample metadata fields
View SamplesNutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation.
Dynamic O-GlcNAc cycling at promoters of Caenorhabditis elegans genes regulating longevity, stress, and immunity.
No sample metadata fields
View SamplesNutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation.
Dynamic O-GlcNAc cycling at promoters of Caenorhabditis elegans genes regulating longevity, stress, and immunity.
No sample metadata fields
View SamplesNutrient-driven O-GlcNAcylation of key components of the transcription machinery may epigenetically modulate gene expression in metazoans. Knockouts of the O-GlcNAc cycling enzymes in C. elegans are viable and fertile, allowing a global analysis of the impact of GlcNAcylation. Here we compare gene expression in wild type and O-GlcNAc mutants (ogt-1 and oga-1) in synchronized, fed L1 animals.
Dynamic O-GlcNAc cycling at promoters of Caenorhabditis elegans genes regulating longevity, stress, and immunity.
No sample metadata fields
View SamplesHomeostasis of the gut microbiota is pivotal to the survival of the host. Intestinal T cells and Innate Lymphoid cells (ILCs) control the composition of the microbiota and respond to its perturbations. Interleukin 22 (IL-22) plays a pivotal role in the immune control of gut commensal and pathogenic bacteria and is secreted by a heterogeneous population of intestinal T cells, NCR- ILC3 and NCR+ILC3. Expression of NCR by ILC3 is believed to define an irreversible effector ILC3 end-state fate in which these cells are key to control of bacterial infection via their production of IL-22. Here we identify the core transcriptional signature that drives the differentiation of NCR- ILC3 into NCR+ ILC3 and reveal that NCR+ILC3 exhibit more plasticity than originally thought, as NCR+ ILC3 can revert to NCR- ILC3. Contrary to the prevailing understanding of NCR+ ILC3 genesis and function, in vivo analyses of mice conditionally deleted of the key ILC3 genes Stat3, Il22, Tbet and Mcl1 demonstrated that NCR+ ILC3 were not essential for the control of colonic infections in the presence of T cells. However, NCR+ ILC3 were mandatory for homeostasis of the caecum. Our data identify that the interplay of intestinal T cells and ILC3 results in robust complementary fail-safe mechanisms that ensure gut homeostasis. Overall design: Transcriptional profiling of wild-type and T-bet knockout innate lymphoid cells (ILC3) using RNA sequencing
Complementarity and redundancy of IL-22-producing innate lymphoid cells.
Specimen part, Cell line, Subject
View SamplesWe deep sequenced chromatin-associated RNAs (CARs) from human fibroblast (HF) cells. This resulted in the identification of 141 intronic regions and 74 intergenic regions harbouring CARS. Overall design: We purified CARs from normal HFs by isolating soluble chromatin after MNase treatment, followed by separation of chromatin fragments of different lengths on a sucrose gradient. CARs were converted into double-stranded cDNAs and sequenced using the Illumina Genome Analyzer I.
Characterization of the RNA content of chromatin.
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View SamplesOriginal patient tumor is directly implanted in mice xenografts. Tumor is propagated to multiple mice for conduct of 6 arm treatment trials and control. Therapies are selected based on T0 and F0 genomic profiles.
Using a rhabdomyosarcoma patient-derived xenograft to examine precision medicine approaches and model acquired resistance.
No sample metadata fields
View SamplesUterine double conditional inactivation of Smad2 and Smad3 in mice results in endometrial dysregulation, infertility, and uterine cancer. Smad2/3 cKO mice demonstrate abnormal expression of genes involved in inflammation, cell-cycle checkpoint, migration, steroid biosynthesis, and SMAD1/5-driven genes. We performed RNA-sequencing to identify the gene expression differences between the uterine epithelium of control and Smad2/3 cKO. To control for estrous cycle variations, the uterine epithelium was collected from mice at 0.5 dpc. Global gene expression profiles of Smad2/3 cKO versus control mice was analyzed. Our RNA sequencing analysis was performed at 6 weeks of life and already showed significant differences in migratory (Agr2,Slit2) and inflammatory (Ccl20, Crispld2) markers between Smad2/3 cKO and control mice. Overall design: Two group comparison: uterine epithelium of control and Smad2/3 cKO mice. We generated a conditional knockout of Smad2/3 in the uterus and demonstrated that Smad2/3 plays a critical role in the endometrium, with disruption resulting in pubertal-onset uterine hyperplasia and ultimately fatal uterine cancer.
Uterine double-conditional inactivation of <i>Smad2</i> and <i>Smad3</i> in mice causes endometrial dysregulation, infertility, and uterine cancer.
Specimen part, Subject
View SamplesUpon pathogenic infection, drosophila larval host mounts an immune response. Parasitic wasps inject venom that contain virulence factors during oviposition, which can elicit host immune response, and in some cases, suppress host immune responses altogether. Several microarray experiments have been performed on different classes of parasitic wasps. We wanted to compare how Ganaspis xanthopoda-infected hosts respond compared to other classes of parasitic wasps.
A database for the analysis of immunity genes in Drosophila: PADMA database.
Time
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