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GSE35139
Mus musculus
28 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We identified a congenic mouse with an introgressed region from the A/J donor inbred strain on an inbred C57BL/6J background that showed a reduced locomotor stimulant response to methamphetamine. We conducted microarray analysis of the striatum from drug-naive female and male mice that were 6-9 weeks old. The congenic region is on chromosome 11 and spans approximately 84-96 Mb. There were two groups of mice used in the analysis: B6 control mice versus congenic mice. Congenic mice were collapsed across heterozygous and homozygous genotypes.
Publication Title
Congenic dissection of a major QTL for methamphetamine sensitivity implicates epistasis.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 30 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
About 15% of the TG26 mice develop lymphoma. HIV protein expression is observed, particularly the protein p17/Matrix. Total cellular RNA from spleen and lymph nodes from 3 groups of animals: FVB/N controls (n=3), Tg26 asymptomatic (n=6), and Tg26 with lymphoma (n=6). Results provide insights into the gene expression program in animals with lymphoma.
Publication Title
Expression of HIV-1 matrix protein p17 and association with B-cell lymphoma in HIV-1 transgenic mice.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Expression 430B Array (moe430b), Affymetrix Mouse Expression 430A Array (moe430a)
Description
Comparison of R1 embryonic stem cells response to DMSO and retinoic acid and control
Publication Title
Meta-analysis of differentiating mouse embryonic stem cell gene expression kinetics reveals early change of a small gene set.
Sample Metadata Fields
Specimen part, Cell line, Compound
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Urothelial cell carcinoma of the bladder (UCC) is a common disease characterized by FGFR3 mutation. Whilst upregulation of this oncogene occurs most frequently in low-grade non-invasive tumors, recent data reveal increased FGFR3 expression characterizes a common sub-type of invasive UCC sharing genetic similarities with lobular breast cancer. These similarities include upregulation of the FOXA1 transcription factor and reduced expression of microRNAs-99a/100. We have previously identified direct regulation of FGFR3 by these two microRNAs and now search for further targets. Using a microarray meta-database we find potential FOXA1 regulation by microRNAs-99a/100. We confirm direct targeting of the FOXA1 3UTR by microRNAs-99a/100 and also potential indirect regulation through microRNA-485-5p/SOX5/JUN-D/FOXL1 and microRNA-486/FOXO1a. In 292 benign and malignant urothelial samples, we find an inverse correlation between the expression of FOXA1 and microRNAs-99a/100 (r=-0.33 to -0.43, p<0.05). As for FGFR3 in UCC, tumors with high FOXA1 expression have lower rates of progression than those with low expression (Log rank p=0.009). Using global gene expression and CpG methylation profiling we find genotypic consequences of FOXA1 upregulation in UCC. These are associated with regional hypomethylation and near FOXA1 binding sites, and mirror patterns previously reported in FGFR3 mutant UCC. These include gene silencing through aberrant hypermethylation (e.g. IGFBP3) and affect genes that characterize lobular breast cancer (e.g. ERBB2, XBP1). In conclusion, we have identified microRNAs-99a/100 mediate a direct relationship between FGFR3 and FOXA1, and potentially facilitate cross talk between these pathways in UCC.
Publication Title
MicroRNA-99a and 100 mediated upregulation of FOXA1 in bladder cancer.
Sample Metadata Fields
Cell line
View Samples- Macaca mulatta
- 19 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Rhesus macaques (Macaca mulatta) infected with a lethal dose of lymphocytic choriomeningitis virus-strain WE (LCMV-WE) provide a model for Lassa fever virus infection of man. Like Lassa fever in human beings, disease begins with flu-like symptoms but can progress to morbidity fairly rapidly. Previously, we profiled the blood transcriptome of LCMV-infected monkeys (M. Djavani et al. J. Virol. 2007: PMID 17522210) showing distinct pre-viremic and viremic stages that discriminated between virulent and benign infections. In the present study, changes in liver gene expression from macaques infected with virulent LCMV-WE were compared to gene expression in uninfected monkeys as well as to monkeys that were infected but not diseased. We observed gene expression changes that occurred before the viremic stage of the disease, and could potentially serve as biomarkers that discriminate between exposure to a hemorrhagic fever virus and exposure to a benign virus. Based on a functional pathway analysis of differentially expressed genes, virulent LCMV-WE had a much broader effect on liver cell function than non-virulent virus. During the first few days of infection, virulent virus impacted gene expression associated with the generation of energy, such as fatty acid metabolism and glucose metabolism, with the complement and coagulation cascades, and with steroid metabolism, MAPK signaling and cell adhesion. For example, the energy profile resembled that of an organism entering starvation: acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis, was shut down and gene products involved in gluconeogenesis were up-regulated. In conclusion, this study identifies several potential gene markers of LCMV-WE-associated liver disease and contributes to the database of gene expression changes correlated with LCMV pathogenesis in primates.
Publication Title
Gene expression in primate liver during viral hemorrhagic fever.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
The MYC transcription factor is a master regulator of diverse cancer pathways and somatic cell reprogramming. MYC is a compelling therapeutic target that exhibits cancer-specific cellular effects. Pharmacologic inhibition of MYC function has proven challenging due to its numerous modes of forced expression and the difficulty of disrupting protein-DNA interactions. Here we demonstrate the rapid and potent abrogation of MYC gene transcription by representative small molecule bromodomain inhibitors of the BET family of chromatin adaptors. This transcriptional suppression of MYC was observed in the context of the natural, chromosomally translocated, and amplified gene locus. Inhibition of BET bromodomain-promoter interactions and subsequent reduction of MYC transcript and protein levels resulted in G1 arrest and extensive apoptosis in a variety of leukemia and lymphoma cell lines. Exogenous expression of MYC from an artificial promoter that is resistant to BET regulation significantly protected cells from growth suppression by BET inhibitors and revealed that MYC exerts a direct and tight control of key pro-growth and anti-apoptotic target genes. Transcriptional profiling of two cells after 4 and 8 hours of treatment with BET inhibitor shows that both MYC and its targets are strongly down-regulated. We thus demonstrate that pharmacologic inhibition of MYC is achievable through targeting BET bromodomains, and suggest that such inhibitors may have broad clinical applicability given the widespread pathogenetic role of MYC in cancer.
Publication Title
Targeting MYC dependence in cancer by inhibiting BET bromodomains.
Sample Metadata Fields
Cell line, Treatment
View Samples- Bos taurus
- 87 Downloadable Samples
Illumina HiSeq 2000
Description
MicroRNA regulation of the bovine local and systemic monocyte transcriptional responses to an in vivo Streptococcus uberis challenge Overall design: Milk and blood isolated CD14+ monocyte cells taken from 5 infected Holstein friesians and 5 control Holstein friesians. Five animal infected with live S. uberis, cells extracted at 0, 12, 24, 36, and 48 hours post infection.
Publication Title
MicroRNA regulation of bovine monocyte inflammatory and metabolic networks in an in vivo infection model.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Bos taurus
- 94 Downloadable Samples
- Illumina HiSeq 2000
Description
MicroRNAs are amplifiers of monocyte inflammatory networks and repressors of metabolism Overall design: Milk and blood isolated CD14+ monocyte cells taken from 5 infected Holstein friesians and 5 control Holstein friesians. Five animal infected with live S. uberis, cells extracted at 0, 12, 24, 36, and 48 hours post infection.
Publication Title
MicroRNA regulation of bovine monocyte inflammatory and metabolic networks in an in vivo infection model.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Saccharomyces cerevisiae
- 21 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
We used genome-wide expression analyses to study the response of Saccharomyces cerevisiae to stress throughout a 15-day wine fermentation. Forty percent of the yeast genome significantly changed expression levels to mediate long-term adaptation to an environment in which ethanol is both a stressor and a carbon source. Within this set, we identify a group of 223 genes, designated as the Fermentation Stress Response (FSR), that are dramatically and permanently induced; FSR genes exhibited changes ranging from four-to eighty-fold. The FSR is novel; 62% of the genes involved have not been implicated in global stress responses and 28% of the genes have no functional annotation. Genes involved in respiratory metabolism and gluconeogenesis were expressed during fermentation despite the presence of high concentrations of glucose. Ethanol, rather than nutrient depletion, was responsible for entry of yeast cells into stationary phase. Ethanol seems to regulate yeast metabolism through hitherto undiscovered regulatory networks during wine fermentation.
Publication Title
Dynamics of the yeast transcriptome during wine fermentation reveals a novel fermentation stress response.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 112 Downloadable Samples
- Illumina HiSeq 4000
Description
Sensitivity to different pain modalities has a genetic basis that remains largely unknown. The use of closely related inbred mouse strains can facilitate gene mapping of nociceptive behaviors in preclinical pain models. We previously reported enhanced sensitivity to acute thermal nociception in C57BL/6J (B6J) versus C57BL/6N (B6N) substrains. Here, we expanded on pain phenotypes and observed an increase in inflammatory nociceptive behaviors induced by hindpaw formalin injections in B6J versus B6N mice (Charles River Laboratories). No strain differences were observed in mechanical or thermal hypersensitivity or in paw diameter following the Complete Freund s Adjuvant (CFA) model of inflammatory pain, indicating specificity in the inflammatory nociceptive stimulus. In the chronic nerve constriction injury (CCI), a model of neuropathic pain, no strain differences were observed in baseline mechanical threshold or in mechanical hypersensitivity up to one month post-CCI. We replicated the enhanced thermal nociception in B6J mice in the 52.5 C hot plate test relative to B6N mice from The Jackson Laboratory. Using a B6J x B6N-F2 cross (N=164), we mapped a major QTL underlying hot plate sensitivity to chromosome 7 that peaked at 26 Mb (LOD = 3.81, 8.74 Mb-36.50 Mb) that was more pronounced in males. Genes containing expression QTLs (eQTLs) associated with the peak nociceptive marker that have been implicated in pain and inflammation include Ryr1, Cyp2a5, Pou2f2, Clip3, Sirt2, Actn4, and Ltbp4 (FDR < 0.05). Future studies involving positional cloning and gene editing will determine the quantitative trait gene(s) and potential pleiotropy of this locus across other pain modalities. RNA-seq data and genotype information from striatum punches of F2 C57BL/6J (B6J) cross C57BL/NJ (B6NJ) oxycodone-treated mice. Genotypes are given relative to B6J allele, eg 0 = homozygous B6J. Overall design: C57BL/6J (B6J) and C57BL/NJ (B6NJ) mice were purchased from JAX at 7 weeks of age and were habituated in the vivarium one week prior to experimental testing that occurred next door. B6J females were crossed to B6NJ males to generate B6J x B6NJ-F1 mice and B6J x B6NJ F1 offspring were intercrossed to generate B6J x B6NJ F2 mice. Mice were 50-100 days old at the time of testing. F2 mice recieved four daily oxycodone injections (20 mg/kg, i.p.). Ninety SNP markers spaced approximately 30 Mb (approximately 15 cM) apart were genotyped using a custom-designed Fluidigm array.
Publication Title
C57BL/6 substrain differences in inflammatory and neuropathic nociception and genetic mapping of a major quantitative trait locus underlying acute thermal nociception.
Sample Metadata Fields
Sex, Age, Subject
View Samples