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GSE63205
Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Scope: Soy flour diet (MS) prevented isoflavones from stimulating MCF-7 tumor growth in athymic nude mice, indicating that other bioactive compounds in soy can negate the estrogenic properties of isoflavones. The underlying signal transduction pathways to explain the protective effects of soy flour consumption were studied here.
Publication Title
Isoflavones in soy flour diet have different effects on whole-genome expression patterns than purified isoflavone mix in human MCF-7 breast tumors in ovariectomized athymic nude mice.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 9 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Mutation of MTF in Arabidopsis increases Agrobacterium-mediated transformation susceptibility. Being a putative transcription factor, different genes controlling transformation may be regulated by MTF.
Publication Title
Cytokinins secreted by Agrobacterium promote transformation by repressing a plant myb transcription factor.
Sample Metadata Fields
Specimen part
View Samples- Glycine max
- 22 Downloadable Samples
Illumina HiScanSQ
Description
Phytophthora root and stem rot (PRR) of soybean, caused by Phytophthora sojae, is effectively controlled by Rps genes in soybean. Rps genes are race-specific, yet the mechanism of resistance, as well as susceptibility, remains largely unclear. Taking advantage of RNA-seq technology, we sequenced the transcriptomes of 10 near isogenic lines (NIL), each with a unique Rps gene, and the recurrent susceptible parent 'Williams'. A total of 4330 differentially expressed genes (DEGs) were identified in 'Williams' while 2075 to 5499 DEGs were identified in each NIL. Comparisons between the NILs and 'Williams' allowed classification of two major groups of DEGs of interest: incompatible reaction associated genes (IRAGs) and compatible reaction associated genes (CRAGs). Hierarchical cluster analysis divided NILs into three clusters: Cluster I (Rps1-a), Cluster II (Rps1-b, 1-c and 1-k) and Cluster III (Rps3-a, 3-b, 3-c, 4, 5, and 6). Heatmap analysis, along with GO analysis suggested that the diversity of clusters for NILs were likely due to variation of the number of DEGs and the intensity of gene expression, rather than functional differentiation. Further analysis suggested that transcription factors might play pivotal role in determination of the cluster pattern, and that WRKY family were strongly associated with incompatible reactions. Analysis of IRAGs and CRAGs with putative functions suggested that the regulation of many phytohormone signaling pathways were associated with incompatible or compatible interactions with potential crosstalk between each other. As such, our study provides an in depth view of both incompatible and compatible interactions between soybean and P. sojae, which provides further insight into the mechanisms involved in host-pathogen interactions. Overall design: 22 samples were sequenced, 11 inoculated with P. sojae, the other 11 were mock-inoculated
Publication Title
Molecular response to the pathogen Phytophthora sojae among ten soybean near isogenic lines revealed by comparative transcriptomics.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 93 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of young adult mice treated with a single systemic dose of MAM display DNA damage (O6-methylguanine lesions) that peaks at 48 hours and decline to near-normal levels at 7 days post-treatment. By contrast, at this time, MAM-treated mice lacking the gene encoding the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT), showed persistent O6-methylguanine DNA damage. The DNA damage was linked to cell-signaling pathways that are perturbed in cancer and neurodegenerative disease. These data are consistent with the established carcinogenic and developmental neurotoxic properties of MAM in rodents, and they support the proposal that cancer and neurodegeneration share common signal transduction pathways. They also strengthen the hypothesis that early life exposure to the MAM glucoside cycasin has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for medicine and/or food. Exposure to environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimers disease, as well as cancer.
Publication Title
The cycad genotoxin MAM modulates brain cellular pathways involved in neurodegenerative disease and cancer in a DNA damage-linked manner.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Nrf2 Modulates Host Defense during Streptococcus pneumoniae Pneumonia in Mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
The transcription factor Nrf2 (gene symbol Nfe2l2) regulates the transcriptional response to oxidative stress and plays a critical protective role in the lungs.
Publication Title
Nrf2 Modulates Host Defense during Streptococcus pneumoniae Pneumonia in Mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
The transcription factor Nrf2 (gene symbol Nfe2l2) regulates the transcriptional response to oxidative stress and plays a critical protective role in the lungs.
Publication Title
Nrf2 Modulates Host Defense during Streptococcus pneumoniae Pneumonia in Mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 79 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Network analysis reveals centrally connected genes and pathways involved in CD8+ T cell exhaustion versus memory.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
During acute viral infections, nave CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become exhausted and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.
Publication Title
Network analysis reveals centrally connected genes and pathways involved in CD8+ T cell exhaustion versus memory.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
MicroRNA-155 (miR-155) is upregulated in primary effector CD8 T cells but is expressed at low amounts in nave cells. Anti-viral CD8 T cell responses and viral clearance were impaired in miR-155 deficient (bic-/-) mice, and this defect was intrinsic to CD8 T cells, as adoptively transferred bic-/- CD8 T cells generated greatly reduced primary and memory responses during infection. To understand the mechanism by which miR-155 regulates CD8 T cell activation, we analyzed the gene expression profiles of naive and in vitro activated wild-type and bic-/- CD8 T cells.
Publication Title
The microRNA miR-155 controls CD8(+) T cell responses by regulating interferon signaling.
Sample Metadata Fields
Specimen part
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