We hypothesize that gene expression in the Type II cells of Nrf2+/+ and Nrf2-/- mice are divergent thus contributing the cell growth. More specifically, type II cells from Nrf2-/- mice have increased reactive oxygen species that cause the impaired cell growth. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Nrf2+/+ and Nrf2-/- cells.
Genetic dissection of the Nrf2-dependent redox signaling-regulated transcriptional programs of cell proliferation and cytoprotection.
No sample metadata fields
View SamplesThe goal of this study was to examine whether immune responses to Plasmodium chabaudi infection differ between the sexes and are altered by the presence of gonadal steroids. Gonadally-intact males were more likely than intact females to die following P. chabaudi infection, exhibit slower recovery from infection-associated weight loss, hypothermia, and anemia, have reduced IFN-associated gene expression and IFN production during peak parasitemia, and produce less antibody during the recovery phase of infection. Gonadectomy of male and female mice altered these sex-associated differences, suggesting that sex steroid hormone, in particular androgens and estrogens, may modulate immune responses to infection.
Involvement of gonadal steroids and gamma interferon in sex differences in response to blood-stage malaria infection.
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View SamplesGene expression profiles were examined in whole lung tissue collected from male and female Long-Evans rats at different time points after inoculation with Seoul virus (i.e., the species-specific hantavirus that infects Norway rats)
Sex differences in the recognition of and innate antiviral responses to Seoul virus in Norway rats.
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View SamplesE2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors
Estrogenic compounds reduce influenza A virus replication in primary human nasal epithelial cells derived from female, but not male, donors.
Sex, Specimen part, Treatment
View SamplesThe functions of key oncogenic transcription factors independent of context have not been fully delineated despite our richer understanding of the genetic alterations in human cancers. The MYC oncogene, which produces the Myc transcription factor, is frequently altered in human cancer and is a major regulatory hub for many cancers. In this regard, we sought to unravel the primordial signature of Myc function by using high-throughput genomic approaches to identify the cell-type independent core Myc target gene signature. Using a model of human B lymphoma cells bearing inducible MYC, we identified a stringent set of direct Myc target genes via chromatin immunoprecipitation (ChIP), global nuclear run-on assay, and changes in mRNA levels. We also identified direct Myc targets in human embryonic stem cells (ESCs). We further document that a Myc core signature (MCS) set of target genes is shared in mouse and human ESCs as well as in four other human cancer cell types. Remarkably, the expression of the MCS correlates with MYC expression in a cell-type independent manner across 8,129 microarray samples, which include 312 cell and tissue types. Furthermore, the expression of the MCS is elevated in vivo in Em-Myc transgenic murine lymphoma cells as compared with premalignant or normal B lymphocytes. Expression of the MCS in human B cell lymphomas, acute leukemia, lung cancers or Ewing sarcomas has the highest correlation with MYC expression. Annotation of this gene signature reveals Myc's primordial function in RNA processing, ribosome biogenesis and biomass accumulation as its key roles in cancer and stem cells.
Cell-type independent MYC target genes reveal a primordial signature involved in biomass accumulation.
Specimen part, Cell line, Treatment
View SamplesTo compare hepatic gene expression in conditional Keap1 knockout (Alb-Cre:Keap1(flox/-)) and genetic control mice. Disruption of Keap1-mediated repression of Nrf2 signaling was expected to result in increased expression of Nrf2-regulated genes.
Genetic or pharmacologic amplification of nrf2 signaling inhibits acute inflammatory liver injury in mice.
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View SamplesP493-6 contain a tet repressible MYC contruct. In the presense of tetracycline, MYC levels are great reduced and the cells cease to cycle. Gene expression was compared between high and low MYC expressing cells
Cell-type independent MYC target genes reveal a primordial signature involved in biomass accumulation.
Cell line, Treatment
View SamplesIn this dataset, we studied human dopaminergic neuron differenation from induced pluripotent stem cells (iPSCs). We included the gene expression data obtained from iPSCs and iPSC-derived dopaminergic neurons.
No associated publication
Specimen part
View SamplesThis study aims at using RNA-Seq to characterize effects of ribavirin on whole transcriptomes of S. cerevisiae strains containing dsRNA virus-like particles.
No associated publication
Specimen part, Disease, Cell line
View SamplesTo investigate the early host response triggered by three different strains of Trypanosoma cruzi at a local infection site, changes in host gene expression were monitored in a murine intradermal infection model using Affymetrix oligonucleotide arrays. Robust induction of IFN-stimulated genes (ISGs) was observed in excised skin 24 hours post-infection where the level of ISG induction was parasite strain-dependent with the least virulent strain triggering a muted IFN response. Infection of mice immunodepleted of IFN-producing cells or infection of IFN-deficient mice had minimal impact on the IFN response generated in T. cruzi infected mice. In contrast, infection of mice lacking the type I IFN receptor demonstrated that type I IFNs are largely responsible for the IFN response generated at the site of infection. These data highlight type I IFNs as important components of the innate immune response to T. cruzi the site of inoculation and their role in shaping the early transcriptional response to this pathogen.
No associated publication
No sample metadata fields
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