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GSE12584
Hordeum vulgare, Hordeum vulgare subsp. spontaneum
18 Downloadable Samples
Affymetrix Barley Genome Array (barley1)
Description
The bird cherry-oat aphid (Rhopalosiphum padi L.) (Homoptera: Aphididae) is an important pest on cereals causing plant growth reduction but no specific leaf symptoms. Breeding of barley (Hordeum vulgare L.) for R. padi resistance shows that there are several resistance genes involved, reducing aphid growth. In an attempt to identify candidate sequences for resistance-related genes, we performed a microarray analysis of gene expression after two days of aphid infestation in two susceptible barley lines and two genotypes with partial resistance. One of the four lines is a descendant of two of the other genotypes. The analysis revealed large differences in gene induction between the four lines, indicating substantial variation in response even between closely related genotypes. Genes induced in the aphid-infested tissue were mainly related to defence, primary metabolism and signalling. Only twenty-four genes were induced in all lines, none of them related to oxidative stress or secondary metabolism. Few genes were down-regulated and none of those was common to all four lines. There were differences in aphid-induced gene regulation between resistant and susceptible lines, and results from control plants without aphids also revealed differences in constitutive gene expression between the two types of lines. Candidate sequences for both induced and constitutive resistance factors have been identified, among them a proteinase inhibitor, a Ser/Thr kinase and several thionins.
Publication Title
Microarray analysis of the interaction between the aphid Rhopalosiphum padi and host plants reveals both differences and similarities between susceptible and partially resistant barley lines.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We used microarrays to compare the gene expression profiles of different H1N1 isolates (seasonal and pandemic) in lung epithelial cells in vitro.
Publication Title
Early host responses of seasonal and pandemic influenza A viruses in primary well-differentiated human lung epithelial cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 19 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The C57BL/6.NOD-Aec1Aec2 mouse is a model for primary Sjgrens syndrome and was constructed by introducing two genetic intervals derived from the NOD mouse that confers Sjgrens syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice.
Publication Title
Transcriptional landscapes of emerging autoimmunity: transient aberrations in the targeted tissue's extracellular milieu precede immune responses in Sjögren's syndrome.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
Illumina Genome Analyzer, Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer
Description
Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNFalpha can facilitate tumor progression and metastasis. However, our knowledge of the molecular mechanisms underlying TNBC progression mediated by inflammation is still limited. Here, we define the AP-1 transcription factor c-Jun cistrome, which is comprised of 13800 binding sites responsive to TNFalpha-induced signaling in TNBC cells. In addition, we show that c-Jun regulates nearly a third of the TNFalpha-elicited transcriptome. Expression of the c-Jun-regulated pro-invasion gene program is strongly associated with clinical outcomes in TNBCs. Mechanistically, we demonstrate that c-Jun drives TNFalpha-mediated TNBC tumorigenicity by transcriptional regulation of Ninj1. As exemplified by the c-Jun bound CXC chemokine genes clustered on chromosome 4, we demonstrate that NF-kB might be a pioneer factor and is required for the regulation of TNFalpha-inducible inflammatory genes, whereas c-Jun has little effect. Together, our results uncover AP-1 as an important determinant for inflammation-induced cancer progression, rather than inflammatory response.
Publication Title
AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Fibroblast growth factor-23 (FGF23), a circulating protein produced in bone, causes renal inorganic phosphate (Pi) wasting by down-regulation of sodium phosphate co-transporter 2a (Npt2a). The mechanism behind this action is unknown. We have previously generated transgenic mice (TG) expressing human wild-type FGF23 under the control of the 1 (I) collagen promoter. In this study we performed a large scale gene expression study of kidneys from TG mice and wild-type littermates. Several genes that play a role in Pi regulation had decreased expression levels, such as Npt2a, but also Pdzk1 which is a scaffolding protein known to interact with NPT2a. Importantly, the Klotho gene, a suggested crucial co-factor for FGF23 receptor binding and activation, was the most affected decreased gene. However, other genes proposed to regulate Pi levels, such as secreted Frizzled Related Protein 4 (sFRP4), Na+/H+ exchanger regulatory factor 1 (NHERF1) and the FGF-receptors 1-4, revealed no changes. Interestingly, expression levels of inflammatory response genes were increased and histological analysis revealed tubular nephropathy in the TG mice kidneys. In conclusion, FGF23 TG mice have altered kidney gene expression levels of several genes thought to be part of Pi homeostasis and an increase in inflammatory response genes, data supported by histological analysis. These findings may lead to further understanding of how FGF23 mediates its actions on renal Pi regulation.
Publication Title
Gene expression analysis of kidneys from transgenic mice expressing fibroblast growth factor-23.
Sample Metadata Fields
Age
View Samples- Bos indicus, Bos taurus
- 6 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
This trial was undertaken to examine the perhipheral cellular and antibody response of cattle following infestation with the cattle tick, Rhipicephalus microplus. The information from the Affymetrix gene expression data is used to complement other measurements of immune function such as cellular subset composition and antibody response in cattle of high (Brahman) and low (Holstein-Friesian) resistance to the cattle tick.
Publication Title
Immunological profiles of Bos taurus and Bos indicus cattle infested with the cattle tick, Rhipicephalus (Boophilus) microplus.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genome-wide profiling of AP-1-regulated transcription provides insights into the invasiveness of triple-negative breast cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina Genome Analyzer
Description
Triple negative breast cancer (TNBC) is an aggressive clinical phenotype, and accounts for 15% to 20% of all breast cancers. The molecular determinants of malignant cell behaviors in TNBC remain largely unknown. We find that the AP-1 transcription factor component, Fra-1, is overexpressed in basal-like breast tumors, and its expression level has high prognostic significance. Depletion of Fra-1 or its heterodimeric partner c-Jun inhibits the proliferative and invasive phenotypes in TNBC cells. To gain insights into the transcriptional regulatory networks of AP-1 in TNBC cells, we combine genome-wide ChIP-seq with loss-of-function transcriptome analyses. We observe dysregulation of direct targets of the Fra-1/c-Jun heterodimer involved in cell proliferation, cell adhesion, and cell-cell contact. Intriguingly, we find that AP-1 mediates downregulation of E-cadherin through direct transcriptional induction of ZEB2. This work sheds light on the mechanisms and pathways by which TNBC acquires invasiveness and proliferative propensity.
Publication Title
Genome-wide profiling of AP-1-regulated transcription provides insights into the invasiveness of triple-negative breast cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Pan troglodytes, Homo sapiens
- 23 Downloadable Samples
- Sentrix HumanRef-8 v2 Expression BeadChip
Description
The signaling pathways orchestrating both the evolution and development of language in the human brain remain unknown. To date, the transcription factor FOXP2 is the only gene implicated in Mendelian forms of human speech and language dysfunction1,2. It has been proposed, that the amino acid composition in the human variant of FOXP2 has undergone accelerated evolution, and this change occurred around the time of language emergence in humans3,4. However, this remains controversial, and whether the acquisition of these amino acids in human FOXP2 has any functional consequence in human neurons remains untested. Here, we demonstrate that these two amino acids confer new functionality in terms of differential transcriptional regulation, and extend these observations to in vivo brain, showing that several of the differential FOXP2 targets significantly overlap with genes different between human and chimpanzee brain. We also identify novel relationships among the differentially expressed genes with additional critical regulators of neuronal development. These data provide support for the functional relevance of changes that occur on the human lineage by showing that the two amino acids unique to human FOXP2 can lead to significant differences in gene expression patterns across brain evolution, with direct consequences for human brain development and disease. Since FOXP2 has an important role in the use of language in humans, the identified targets may have a critical function in the development and evolution of language circuitry in humans.
Publication Title
Human-specific transcriptional regulation of CNS development genes by FOXP2.
Sample Metadata Fields
Specimen part, Cell line
View Samples