Transcriptional profiles in the HdhQ150 mouse model of HD and wild-type litter mates at 6, 12 and 18 months
Longitudinal analysis of gene expression and behaviour in the HdhQ150 mouse model of Huntington's disease.
Sex, Age, Specimen part
View SamplesGene expression profiles of a single Arabidopsis genotype (Col-0) in response to isogenic Pseudomonas syringae strains expressing one of four different cloned avr genes was studied (avrRpt2, avrRpm1, avrPphB, avrRps4; responses mediated by the R genes RPS2, RPM1, RPS5 and RPS4 ).
Discovery of ADP-ribosylation and other plant defense pathway elements through expression profiling of four different Arabidopsis-Pseudomonas R-avr interactions.
Age, Specimen part, Disease, Disease stage
View SamplesTo investigate the systemic molecular changes occurring as a result of Dhr96 knockdown or over-expression, a comparison between knockdown or overexpression lines and their genetic controls were performed. 0-3 day old adult males or females were reared on 3 separate batches of diet (this was the standard diet we used for culturing Drosophila melanogaster and was made up of 10L water, 100g agar (USP #7060 Bio-serve), 350g Brewers dried yeast (Sunshine Health), 300g black treacle (Lyles), 150g sucrose (Tate & Lyle), 300g Difco dextrose (Becton Dickinson), 150g cornmeal (#1151, Bioserve), 100g wheatgerm (#1659, Bioserve), 200g soya bean flour (#S9633 Sigma Aldrich), 10g methyl-4-hydroxybenzoate (#H3647 Sigma Aldrich) in 10ml ethanol, 50ml proprionic acid (#P5561 Sigma Aldrich)). Each of these 3 batches was considered to represent independent biological replication. The RNA samples were hybridized to the Affymetrix Drosophila GeneChip 2.
Insecticide detoxification indicator strains as tools for enhancing chemical discovery screens.
Sex, Specimen part
View SamplesNormal human colorectal mucosa was sampled at points along the colon.
Map of differential transcript expression in the normal human large intestine.
Specimen part
View SamplesHD R6/1 transgenic mouse line brain hemispheres dissected. RNA targets were created for transgenics and wildtypes at time points 18, 22 and 27 weeks. Profiles and data analysis performed using the Bioconductor software and linear model contrasts using LIMMA on RMA probeset summarys.
Brain gene expression correlates with changes in behavior in the R6/1 mouse model of Huntington's disease.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Insecticide detoxification indicator strains as tools for enhancing chemical discovery screens.
No sample metadata fields
View SamplesTo test whether other genes were being silenced in the Cyp6g1 knockdown strain due to off-target RNAi effects, and whether other gene expression changes were contributing to the altered susceptibility to imidacloprid in these knockdown flies. A comparison between w;Act5C-GAL4/CyO; UAS:RNAi_Cyp6g1Hp2/TM3Sb and the genetic control w;Act-GAL4/CyO;+/TM3Sb was performed. Ten 2-3 day old adult males or females were transferred to sugar-agar plates and then collected at various time points (0, 2, 5, 8 hours). The RNA samples for up to three independent experiments per timepoint for each genotype were then pooled, in equal concentrations, before hybridisation to the Affymetrix Drosophila GeneChip 1.
Insecticide detoxification indicator strains as tools for enhancing chemical discovery screens.
Sex, Specimen part, Time
View SamplesBackground: We hypothesized that spleen microarray gene expression profiles analyzed with contemporary pathway analysis software would provide molecular pathways of interest and target genes that might help explain the affect of bcl-2 on improving survival during sepsis.
Surviving sepsis: bcl-2 overexpression modulates splenocyte transcriptional responses in vivo.
Specimen part
View SamplesThe rat models of colorectal cancer (CRC), such as the azoxymethane (AOM) cancer-inducing model, are important tools for researching cancer initiation pathways. However, there is limited understanding of the expression pathways of underlying normal rat colonic epithelium and how this relates to human colonic epithelium. The aim of this study was to study the acute effects of AOM on the gene and pathway expression of the rat's colonic epithelium, whilst contrasting the background normal global expression patterns along the length of the rat as compared to the normal human colonic epithelium.
Genomic homeostasis is dysregulated in favour of apoptosis in the colonic epithelium of the azoxymethane treated rat.
Sex, Specimen part, Treatment
View SamplesHuntingtons disease (HD) is a devastating disease for which currently no therapy is available. It is a progressive autosomal dominant neurodegenerative disorder that is caused by a CAG repeat expansion in the HD gene, resulting in an expansion of polyglutamines at the N-terminal end of the encoded protein, designated huntingtin, and the accumulation of cytoplasmic and nuclear aggregates. Not only is there a loss of normal huntingtin function, upon expansion of the CAG repeat there is also a gain of toxic function of the huntingtin protein and this affects a wide range of cellular processes. To identify groups of genes that could play a role in the pathology of Huntingtons disease, we studied mRNA changes in an inducible PC12 model of Huntingtons disease before and after aggregates became visible. This is the first study to show the involvement Nrf2-responsive genes in the oxidative stress response in HD. Oxidative stress related transcripts were altered in expression suggesting a protective response in cells expressing mutant huntingtin at an early stage of cellular pathology. Furthermore, there was a down-regulation of catecholamine biosynthesis resulting in lower dopamine levels in culture. Our results further demonstrate an early impairment of transcription, the cytoskeleton, ion channels and receptors. Given the pathogenic impact of oxidative stress and neuroinflammation, the Nrf2-ARE signaling pathway is an attractive therapeutic target for neurodegenerative diseases.
Mutant huntingtin activates Nrf2-responsive genes and impairs dopamine synthesis in a PC12 model of Huntington's disease.
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