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Mus musculus
24 Downloadable Samples
Illumina HiSeq 2500
Description
Sickle cell disease (SCD) results from a point mutation in the ß-globin gene forming hemoglobin S (HbS), which polymerizes in deoxygenated erythrocytes, triggering recurrent painful vaso-occlusive crises and chronic hemolytic anemia. Reactivation of fetal Hb (HbF) expression ameliorates these symptoms of SCD. Nuclear factor (erythroid derived-2)–like 2 (Nrf2) is a transcription factor that triggers cytoprotective and antioxidant pathways to limit oxidative damage and inflammation and increases HbF synthesis in CD34+ stem cell–derived erythroid progenitors. We investigated the ability of dimethyl fumarate (DMF), a small-molecule Nrf2 agonist, to activate ?-globin transcription and enhance HbF in tissue culture, murine and primate models. DMF recruited Nrf2 to the ?-globin promoters and the locus control region of the ß-globin locus in erythroleukemia cells, elevated HbF in SCD donor–derived erythroid progenitors, and reduced hypoxia-induced sickling. Chronic DMF administration in SCD mice induced HbF and increased Nrf2-dependent genes to detoxify heme and limit inflammation. This improved hematological parameters, reduced plasma-free Hb, and attenuated inflammatory markers. Chronic DMF administration to nonanemic primates increased ?-globin mRNA in BM and HbF protein in red cells. DMF represents a potential therapy for SCD to induce HbF and augment vasoprotection and heme detoxification Overall design: RNA-Seq of 30 samples
Publication Title
Dimethyl fumarate increases fetal hemoglobin, provides heme detoxification, and corrects anemia in sickle cell disease.
Sample Metadata Fields
Age, Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours.
Publication Title
The transcription factor MEF2C negatively controls angiogenic sprouting of endothelial cells depending on oxygen.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Angiogenesis is defined as the formation of new capillaries by sprouting from preexisting vessels. It is mainly triggered by vascular endothelial growth factor (VEGF) and occurs in the adult primarily in wound healing processes or in pathologic tumor vessel growth. To identify genes specifically triggered by VEGF and involved in the process of angiogenesis, we utilized Affymetrix microarrays hybridized with cRNA of human umbilical vein endothelial cells (HUVEC) stimulated with either the main trigger of angiogenesis, VEGF or a more general mitogenic growth factor, EGF.
Publication Title
The VEGF-induced transcriptional response comprises gene clusters at the crossroad of angiogenesis and inflammation.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE15464- Homo sapiens
- 4 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Angiogenesis, the formation of new capillaries by sprouting from preexisting vessels, is mainly induced by VEGF-A. To identify genes which are induced by VEGF-A in endothelial cells, HUVEC were starved and induced by VEGF-A165 for 30, 60 and 150min. RNA of induced and uninduced cells was isolated and subjected to microarray analysis using Affymetrix microarray.
Publication Title
The VEGF-induced transcriptional response comprises gene clusters at the crossroad of angiogenesis and inflammation.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Homo sapiens
- 66 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Chlamydia trachomatis serovariants are responsible for either Trachoma, the leading cause of infectious blindness or sexually transmitted disease, wherein the endocervix is the most frequently infected site in women. Disease caused by Chlamydia typically involves chronic inflammation and scarring. Recent work with a live-attenuated A2497 plasmid deficient vaccine strain (A2497-) demonstrated protection in nonhuman primates against trachoma and a lack of measurable ocular pathology in A2497- infected monkeys. We therefore performed host cell transcriptome analysis of Hela cells infected with A2497 plasmid-containing (A2497) and A2497- Chlamydia over time. Our results indicate that relative to wild type A2497, the A2497- variant illicits a transcriptome response indicative of lowered inflammation response a delayed apoptosis response, a reduction in immune cell recruitement cytokine expression and a reduction in genes involved in cell proliferation and or fibrosis-like activities. The data provided here suggests a model that may explain how plasmid deficient chlamydia may provide an immuno-protective response without the pathology normally seen with plasmid-containing bacteria.
Publication Title
Transcriptional profiling of human epithelial cells infected with plasmid-bearing and plasmid-deficient Chlamydia trachomatis.
Sample Metadata Fields
Disease, Cell line
View Samples GSE13054- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
HLX was found as a VEGF-A induced gene in HUVEC (B.Schweighofer, submitted). In order to detect genes regulated by HLX HUVEC were infected by recombinant adenovirus expressing HLX for 4, 8, 16 and 32h. RNA was isolated and subjected to microarray analysis using Affymetrix microarray.
Publication Title
The VEGF-regulated transcription factor HLX controls the expression of guidance cues and negatively regulates sprouting of endothelial cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 377 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Intensive lifestyle modification is believed to mediate cardiovascular disease (CVD) risk through traditional pathways that affect endothelial function and progression of atherosclerosis; however, the extent, persistence, and clinical significance of molecular change during lifestyle modification are not well known. Our study reveals that gene expression signatures are significantly modulated by rigorous lifestyle behaviors and track with CVD risk profiles over time.
Publication Title
Intensive cardiovascular risk reduction induces sustainable changes in expression of genes and pathways important to vascular function.
Sample Metadata Fields
Sex, Age
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Gene 1.0 ST Array (elegene10st)
Description
The excessive perchlorate utilization as an oxidizer in rocket propellants and blasting agents had led to the contamination of surface and ground waters. This chemical is known to compete with iodine for binding to the thyroid membrane receptors potentially causing hypothyroidism and fetal retardation in pregnant women. Nevertheless, to date, its biological effects are not completely understood. We have investigated the molecular mechanisms responsive to perchlorate in the nematode C. elegans to nominate a candidate gene for further peruse in the development of a C.elegans perchlorate biosensor. Perchlorate (1 mg/mL) affected the transcriptional response of Regulation of developmental process, growth, defense mechanisms and stress response, among other biological processes.
Publication Title
Perchlorate detection <i>via</i> an invertebrate biosensor.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 48 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Interleukin-17 (IL-17) is essential in host defense against extracellular bacteria and fungi, especially at mucosal sites, but it also contributes significantly to inflammatory and autoimmune disease pathologies. Binding of IL-17 to its receptor leads to recruitment of the adaptor protein CIKS/Act1 via heterotypic association of their respective SEFIR domains and to activation of the transcription factor NF-kB; it is not known whether CIKS and/or NF-kB are required for all gene induction events. Here we report that CIKS is essential for all IL-17 induced immediate-early genes in primary mouse embryo fibroblasts, while NF-kB is profoundly involved. We also identify a novel sub-domain in the N-terminus of CIKS that is essential for IL-17-mediated NF-kB activation. This domain is both necessary and sufficient for the interaction between CIKS and TRAF6, an adaptor required for NF-kB activation. The ability of decoy peptides to block this interaction may provide a new therapeutic strategy for intervention in IL-17-driven autoimmune and inflammatory diseases.
Publication Title
IL-17-induced NF-kappaB activation via CIKS/Act1: physiologic significance and signaling mechanisms.
Sample Metadata Fields
Specimen part, Treatment
View Samples GSE23359- Escherichia coli k-12
- 3 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
BW25113 wild type cells grown to OD = 0.8 in LB, add 2 ug/mL nalidixic acid or 10 ug/mL azlocillin for 90 min. Control was without any antibiotic.
Publication Title
Cryptic prophages help bacteria cope with adverse environments.
Sample Metadata Fields
Treatment
View Samples