The present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-/ null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process.
No associated publication
Specimen part
View SamplesFatal familial insomnia (FFI) is a special subtype of genetic human prion diseases that is caused by the D178N mutation of the prion protein gene (PRNP). In this study, global expression patterns of the thalamus and parietal cortex from three patients with FFI were analyzed by Affymetrix Human Genome U133+ 2.0 chip.
Analyses of the similarity and difference of global gene expression profiles in cortex regions of three neurodegenerative diseases: sporadic Creutzfeldt-Jakob disease (sCJD), fatal familial insomnia (FFI), and Alzheimer's disease (AD).
Sex, Age
View SamplesThe familial or genetic Creutzfeldt-Jakob disease (fCJD or gCJD) is the inherent form of human prion diseases, which accounts for approximately 10-15% of human prion diseases that are caused by mutations of the prion protein gene (PRNP). In this study, the global expression patterns of the parietal cortex from a patient with G114V gCJD were comparatively analyzed with the normal controls by using a commercial human genome expression chip. Totally 8774 genes showed differential expression, among them 2769 genes were upregulated and 6005 ones were downregulated. The reliability of the results was confirmed by the real-time RT-PCR assays for several specific genes. The most differentially expressed genes involved in the functions of regulation of transcription, ion transport, transcription, cell adhesion, signal transduction. The gene associated with gliosis was upregulated and the genes marked for neurons were downregulated, while the transcription of PRNP gene maintained unchanged. 169 different pathways showed significantly changed in the brain of G114V gCJD. The most significantly regulated pathways included that of Alzheimers and Parkinsons disease, oxidative phosphorylation, regulation of actin cytoskeleton, MAPK signaling pathway and proteasome, which were described in prion diseases previously. In addition, some rarely addressed pathways in prion diseases, such as axon guidance, gap junction and purine metabolism, were also significantly changed in G114V gCJD. The transcriptional situations of the most genes in the top ten changed pathways were down-regulated. The extensive reductions of gene expressions in G114V gCJD showed the comparable profiles with sporadic CJD. The data here raised the useful clues for understanding the pathogenesis of the disease and selecting the potential biomarkers for diagnostic and therapeutic tools.
No associated publication
Age, Specimen part
View SamplesRotavirus infection is the single most important cause of severe diarrhea in young children worldwide. We used Affymetrix Human U95Av2 high density oligonucleotide arrays to compare gene expression profiles in peripheral blood mononuclear cells (PBMC) of 10 children with acute rotavirus diarrhea and 8 age-matched healthy children. We also examined patterns of gene expression in 5 convalescent-phase PBMC samples from rotavirus patients. For data analysis, we imported .cel files generated by Affymetrix MAS5.0 into Genetraffic 3.1 software (Iobion) and performed robust multi-chip analysis. We considered a gene in patients differentially expressed if its level of expression was at least 1.5-fold higher or lower than the baseline (arithmetic mean) of the corresponding gene in 8 controls and if its pattern of elevated or repressed expression was observed in at least 7 of the 10 patients. Using these criteria, we identified ~1% up- and ~2% down-regulated genes in acute-phase PBMC of patients. Up-regulated genes included those involved in the differentiation, maturation, activation, and survival of B cells, as well as an array of genes with function in inflammatory and antiviral activities. We observed a pattern of repressed expression of a number of genes involved in the various stages of T-cell development and activation. On the basis of these results, we conclude that rotavirus infection induces robust inflammatory response and B-cell activation but represses T-cell response.
Rotavirus infection alters peripheral T-cell homeostasis in children with acute diarrhea.
No sample metadata fields
View SamplesSox31 is a member of the zebrafish SoxB1 subfamily, and its expression can be detected both pre- and post-MBT. To distinguish the function of its maternal and zygotic transcripts, a splice blocking morpholino (Sb MO) was designed to interfere with the processing of new, zygotically synthesised mRNAs without interfering with mRNAs of maternal origin. Developmental arrest was observed in Sb MO which could not bypass MBT.
Splice blocking of zygotic sox31 leads to developmental arrest shortly after Mid-Blastula Transition and induces apoptosis in zebrafish.
No sample metadata fields
View SamplesCHD3 proteins are ATP-dependent chromatin remodeling factors that are components of diverse multisubunit complexes that can either repress or activate gene expression. In plants, the CHD3 protein PICKLE (PKL) is necessary for repression of seed-specific genes during germination and promotes deposition of the repressive epigenetic mark trimethylation of histone H3 lysine 27 (H3K27me3). It is unknown, however, if PKL acts directly at H3K27me3-enriched loci. We undertook a microarray analysis of 14-day-old plants and found that PKL continues to play an important role in expression of H3K27me3-enriched genes and in specification of developmental identity after germination.
No associated publication
Specimen part
View SamplesGAS2DN could suppress the growth of chronic myeloid leukemia cells, including K562, MEG-01 and CD34+ cells from patients. In addition, GAS2DN inhibited the tumorigenic ability of MEG-01 cells in nude mice. To understand the molecular insight of this inhibitory effect of GAS2DN, global gene expression were performed.
No associated publication
Cell line
View SamplesIdentify the PDX model of DLBCL subtypes by the microarray expression profiling
No associated publication
Specimen part, Subject
View SamplesHepatitis E virus (HEV) is an important causative pathogen of acute hepatitis. Because of the absence of an in vitro culture system for HEV, research has been greatly impeded. And interaction between HEV and host cells was mainly studied by tansfection/transinfection system, such as Adeno virus transinfection system. We developed an in vitro culture system for HEV in PLC/PRF/5 cells. With this in vitro culture system, we studied the gene expression profile change by HEV infection.
Hepatitis E genotype 4 virus from feces of monkeys infected experimentally can be cultured in PLC/PRF/5 cells and upregulate host interferon-inducible genes.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of genes with a correlation between copy number and expression in gastric cancer.
Sex, Age, Specimen part, Disease, Disease stage
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