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E-MEXP-459
Mus musculus
15 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
We undertook a survey of gene expression changes in primary microglial cultures with and without neurovirulent (FrCasE) and non-neurovirulent (Fr57E) virus infection to identify physiological changes that could be relevant to the induction of spongiform neurodegeneration. These gene expression analyses were performed using Affymetrix 430A mouse GeneChips (5 chips for each of the three experimental conditions, representing over 14,000 murine genes and ESTs. RNA from 5 separate microglial culture preparations were analyzed for Control (mock infected), Fr57E-, and FrCasE-infected microglia. Present/absent calls were based on MicroArray Suite 5.0 from Affymetrix. Affymetrix CEL files were analyzed using dChip software after normalization of the data between all 15 arrays. Statistical analyses were performed using ANOVA.
Publication Title
Gene expression profiling of microglia infected by a highly neurovirulent murine leukemia virus: implications for neuropathogenesis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 27 Downloadable Samples
IlluminaHiSeq2500
Description
Tick-borne flaviviruses (TBFVs) are ss(+)RNA viruses that cause febrile illnesses, which may progress to severe encephalitis and/or death in humans globally. 30—60% of people who recover from severe acute disease continue to suffer debilitating neurological sequelae due to viral persistence, neurological cell damage incurred during infection and/or host response, or a combination of these. When TBFVs infect mammalian cells in vitro, an acute phase characterized by dramatic apoptosis ensues and kills >95% of infected cells by day 5. Upon refreshing the cell growth medium, surviving cells repopulate and become persistently infected for extended periods of time. However, molecular mechanisms responsible for the initiation and maintenance of viral persistence in vivo and in vitro remain vague. We used unbiased deep sequencing of the HEK 293T cell transcriptome to determine the profiles of acutely infected cells at selected time points as well as of persistently infected cells. Many genes were significantly differentially expressed during the course of the acute phase, but 451 genes were significantly differentially expressed uniquely in persistently infected cells. Ingenuity Pathways Analysis of these genes suggested that the oncogenes AKT2 and ERBB2, which favor cell survival were up-regulated in persistently infected cells, whereas pro-apoptotic genes, such as Bad and IFN-ß1 were down-regulated. There was also an up-regulation of genes encoding antiviral cytokines, such as CCL5, TNF-a and CXCL10 during the acute phase, but these were relatively suppressed in persistently infected cells. Exogenous induction of apoptosis in persistently infected cells with chelerythrine chloride indicated that these cells were resistant to apoptosis in a dose-dependent manner. In summary, the transcriptome profiles of acutely and persistently infected HEK 293T cells are different and evasion of apoptosis is critical for the initiation of TBFV persistence. These results provide a basis for further studying the precise molecular mechanisms of TBFV persistence.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection.
Publication Title
A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 45 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene arrays were used to characterize the global transcriptional alterations in skin biopsy samples of EM lesions in comparison to controls. The transcriptional pattern in EM biopsies consisted of 254 differentially regulated genes (180 induced and 74 repressed) characterized by the induction of chemokines, cytokines, Toll-like receptors, antimicrobial peptides, monocytoid cell activation markers, and numerous genes annotated as interferon (IFN)-inducible. The IFN-inducible genes included 3 transcripts involved in tryptophan catabolism (IDO1, KMO, KYNU) that play a pivotal role in immune evasion by certain other microbial pathogens by driving the differentiation of regulatory T cells.
Publication Title
Transcriptome Assessment of Erythema Migrans Skin Lesions in Patients With Early Lyme Disease Reveals Predominant Interferon Signaling.
Sample Metadata Fields
Specimen part
View Samples- Plasmodium falciparum
- 24 Downloadable Samples
- Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)
Description
Mutations in PfCRT confer chloroquine (CQ) resistance in P. falciparum. Point mutations in the homolog of the mammalian multidrug resistance gene (pfmdr1) can also modulate the levels of CQ response. However, parasites with the same pfcrt and pfmdr1 alleles exhibit a wide range of drug sensitivity, suggesting that additional genes contribute to levels of CQ resistance (CQR).
Publication Title
Genome-wide compensatory changes accompany drug- selected mutations in the Plasmodium falciparum crt gene.
Sample Metadata Fields
No sample metadata fields
View Samples- Staphylococcus aureus
- 24 Downloadable Samples
- Affymetrix S. aureus Genome Array (saureus)
Description
The epidemic character of community-associated methicillin resistant Staphylococcus aureus (CA-MRSA), especially the geographically widespread clone USA300, is poorly understood. USA300 isolates carry a type IV staphylococcal chromosomal cassette mec (SCCmec) element conferring -lactam antibiotic class resistance and a putative pathogenicity island, ACME (arginine catabolic mobile element).
Publication Title
The arginine catabolic mobile element and staphylococcal chromosomal cassette mec linkage: convergence of virulence and resistance in the USA300 clone of methicillin-resistant Staphylococcus aureus.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
CD4+ T cell differentiation into multiple T helper lineages is critical for optimal adaptive immune responses. This report identified a novel intrinsic mechanism by which PD-1 signaling imparted regulatory phenotype to FoxP3+ Th1 cells (denoted as Tbet+iTregPDL1 cells) and iTregs. Tbet+iTregPDL1 cells were capable of preventing inflammation in murine models of experimental colitis and experimental graft versus host disease. PDL-1 binding to PD-1 imparted regulatory function to Tbet+iTregPDL1 cells and iTregs by specifically downregulating an endolysosomal protease asparaginyl endopeptidase (AEP)
Publication Title
PD-1 Inhibitory Receptor Downregulates Asparaginyl Endopeptidase and Maintains Foxp3 Transcription Factor Stability in Induced Regulatory T Cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
To determine the effect of iBET762+, a bromodomain BET inhibitor, on the transcription of 20861 and 20863 cells. These cells are subclones of W12 cells, derived from cervical intraepithelial neoplastic lesion. 20861 contains integrated HPV16 DNA and 20863 contains extrachromosomal HPV16 DNA. iBET762+ decreases expression of the HPV16 E6 and E7 oncogenes in both cell lines and this is expected to have dramatic effects on the cellular transcriptome
Publication Title
Tandemly Integrated HPV16 Can Form a Brd4-Dependent Super-Enhancer-Like Element That Drives Transcription of Viral Oncogenes.
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Essential fatty acids (FA) are not only energy-rich molecules; they are also an important component of the membrane bilayer and recently have been implicated in induction of fatty acid synthase (FAS) and other genes. Using gene chip analysis, we have found that arachidonic acid (AA), an omega-6 fatty acid, induced 11 genes that are regulated by NFkappaB. We verified gene induction by omega-6 fatty acids including COX2, IKBA, NFKB, GMCSF, IL1B, CXCL1, TNFA, IL6, LTA, IL8, PPARG, and ICAM1 using qRTPCR. PGE2 synthesis was increased within 5min of addition of AA. Analysis of upstream signal transduction showed that within 5min of FA addition, phophatidylinositol 3-kinase (PI3K) was significantly activated followed by activation of Akt at 30min. ERK1 and 2, p38, and SAPK/JNK were not phosphorylated after omega-6 FA addition. Thirty minutes after FA addition, we found a significant 3-fold increase in translocation of NFkappaB transcription factor to the nucleus. Addition of non-steroidal anti-inflammatory drug (NSAID) caused a decrease in cox-2 protein synthesis, PGE2 synthesis as well as inhibition of PI3K activation. We have previously shown that AA induced proliferation is also blocked (P<0.001) by PI3K inhibitor LY294002. LY294002 also significantly inhibited the AA induced gene expression of COX2, IL1B, GMCSF, and ICAM1. Taken together, the data suggests that AA via conversion to PGE2 plays an important role in stimulation of growth related genes and proliferation via PI3K signaling and NFkappaB translocation to the nucleus.
Publication Title
Arachidonic acid activates phosphatidylinositol 3-kinase signaling and induces gene expression in prostate cancer.
Sample Metadata Fields
No sample metadata fields
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