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SRP045963
Mus musculus
34 Downloadable Samples
Illumina HiSeq 2000
Description
An increasing number of non-coding RNAs (ncRNAs) are implicated in various human diseases including cancer; however ncRNA transcriptome of hepatocellular carcinoma (HCC) remains largely unexplored. We use CAGE (Cap Analysis of Gene Expression) to comprehensively map transcription start sites (TSSs) across different etiologies of human HCC as well as mouse HCC, with particular emphasis on ncRNAs distant from protein-coding genes. We find thousands of significantly up-regulated distal ncRNAs in HCC tumors compared to their matched non-tumors, which are as many as protein-coding genes. Moreover, we identify many LTR retroviral promoters activated in HCC tissues and expressed in a subfamily-specific manner, which account for approximately 20% of the up-regulated distal ncRNAs. The transcripts derived from LTRs, determined by 3'' RACE, are multi-exon nuclear ncRNAs typically 0.5-2kb in length. This study sheds light on ncRNA transcriptome of human and mouse HCC. Overall design: Expression profiles using CAGE for 37 mouse HCC. The human data are archived at dbGaP (phs000885.v1.p1). An umbrella BioProject has been created to associate the GEO and dbGaP BioProjects: PRJNA278792
Publication Title
Deficiency of multidrug resistance 2 contributes to cell transformation through oxidative stress.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 37 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Acute renal allograft rejection is an important complication in kidney transplantation. Accurate diagnosis of rejection events is necessary for timely response and treatment. We illustrate the usefulness and biological relevance of selected multivariate approaches to detect rejection from genomic and proteomic signals. The data was used to study gene expression changes using whole genome microarray analysis of peripheral blood from subjects with acute rejection (n=20) and non-rejecting controls (n=20) to obtain insight into the molecular and biological causation of acute renal allograft rejection when combined with proteomics (iTRAQ) data for the same patients/time-points.
Publication Title
Novel multivariate methods for integration of genomics and proteomics data: applications in a kidney transplant rejection study.
Sample Metadata Fields
Sex, Specimen part, Race
View Samples- Homo sapiens
- 34 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To determine differential gene expression in peripheral blood of asthmatic individuals undergoing allergen inhalation challenge, post-challenge compared to pre-challenge
Publication Title
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Detecting differential changes in the peripheral whole-blood transcriptome, post-challenge compared to pre-challenge; using non-globin reduced PAXgene (PAX.NGR) tubes
Publication Title
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Detecting differential changes in the peripheral whole-blood transcriptome, post-challenge compared to pre-challenge; using globin reduced PAXgene (PAX.GR) tubes
Publication Title
Peripheral blood gene expression changes during allergen inhalation challenge in atopic asthmatic individuals.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Acute cardiac allograft rejection is a serious complication of heart transplantation. Investigating molecular processes in whole blood via microarrays is a promising avenue of research in transplantation, particularly due to the non-invasive nature of blood sampling. However, whole blood is a complex tissue and the consequent heterogeneity in composition amongst samples is ignored in traditional microarray analysis. This complicates the biological interpretation of microarray data. Here we have applied a statistical deconvolution approach, cell-specific significance analysis of microarrays (csSAM), to whole blood samples from subjects either undergoing acute heart allograft rejection (AR) or not (NR). We identified eight differentially expressed probe-sets significantly correlated to monocytes (mapping to 6 genes, all down-regulated in ARs versus NRs) at a false discovery rate (FDR) <= 15%. None of the genes identified are present in a biomarker panel of acute heart rejection previously published by our group and discovered in the same data.
Publication Title
White blood cell differentials enrich whole blood expression data in the context of acute cardiac allograft rejection.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 136 Downloadable Samples
- IlluminaHiSeq2000
Description
Huntington''s disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals Overall design: mRNA expression profiles were obtained via RNA-seq analysis performed on tissue samples from the cortex of 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals.
Publication Title
Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 96 Downloadable Samples
- Illumina HiSeq 2000
Description
Huntington''s disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 6 and 10 month old knock-in mice with CAG lengths of 20, 50, 92, 140 along with littermate control wild-type animals Overall design: mRNA expression profiles were obtained via RNA-seq analysis performed on samples from the Corpus Striatum tissue of 6 and 10 month old knock-in mice with CAG lengths of 20, 50, 92, 140 along with littermate control wild-type animals.
Publication Title
Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 87 Downloadable Samples
- Illumina HiSeq 2000
Description
Huntington''s disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 6 and 10 month old knock-in mice with CAG lengths of 20, 50, 92, 140 along with littermate control wild-type animals Overall design: mRNA expression profiles were obtained via RNA-seq analysis performed on samples from the Cerebral Cortex tissue of 6 and 10 month old knock-in mice with CAG lengths of 20, 50, 92, 140 along with littermate control wild-type animals.
Publication Title
Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Subject
View Samples