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GSE76096
Mus musculus
12 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
CFTR is a tumor suppressor gene in murine and human intestinal cancer.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 62 Downloadable Samples
Illumina HiSeq 2500
Description
Analysis of the cystic fibrosis gene Cftr in the colon and small intestine of Cftr-deficient murine model. The hypothesis was loss of Cftr altered expression of genes important in intestinal homeostasis and oncogenic signaling pathways. The results identified potential roles of Cftr in up- or down-regulating major gene clusters that belong to groups of immune response, ion channel, intestinal stem cell and other growth regulators. Overall design: The experiments were designed to analyze the role of Cftr-deficiency in tumorigenesis. The goal of this study was to identify genes and pathways associated with Cftr-deficiency in Apc wildtype and ApcMin mice. Total RNAs were isolated from mice, and subjected to deep sequencing, in duplicates, using Illumina HiSeq 2500. Samples that were sequenced in the same batch were analyzed in pair-wise using Tophat-Cuffdiff pipeline as outlined in Nature Protocol from Trapnell C. et al, 2012. The results indicated that Cftr-deficiency overlapped with genes and pathways involved in immune and inflammatory signaling, stem cell regulation, and Wnt/beta catenin signaling. Total RNA was isolated from multiple colon tumors and multiple small intestine tumors from Apc wildtype Cftr-deficient mice, ApcMin Cftr-deficient mice, and ApcMin Cftr wildtype mice. Total RNA was also obtained from Apc wildtype normal colon (epithelial cells) and normal duodenum (whole duodenum minus villi) from three Cftr wildtype and three Cftr-deficient mice. RNA Seq was then conducted on all samples with at least two replicates for each biological sample. Please note that 1) The 23 mice were processed in several batches, and two sequencing runs were carried out at two different dates. Â To control for the batch effect of sequencing, some samples were included in both runs (run1 and run2). 2) To reach the desired sequencing depth and to keep loading balance, each sample was split into halves, and sequenced on two lanes (L007 and L008 for run1, L006 and L007 for run2). therefore, for 11 samples, there are 4 technical replicates, including the 2-batches and 2-lane sequencing method. For the remaining 12 samples, there are 2 technical replicates, referring to the 2-lane sequencing. 3) some of the mice are heterozygous mutant of CFTR gene (CFTRhet), named as "CFTR knockdown".
Publication Title
CFTR is a tumor suppressor gene in murine and human intestinal cancer.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of the cystic fibrosis gene Cftr in the colon and small intestine of Cftr-deficient murine model. The hypothesis was loss of Cftr altered expression of genes important in intestinal homeostasis and oncogenic signaling pathways. The results identified potential roles of Cftr in up- or down-regulating major gene clusters that belong to groups of immune response, ion channel, intestinal stem cell and other growth regulators.
Publication Title
CFTR is a tumor suppressor gene in murine and human intestinal cancer.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 51 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Differencies between groups between pre and post haematopoietic stem cell transplantation children
Publication Title
Genetic Background of Immune Complications after Allogeneic Hematopoietic Stem Cell Transplantation in Children.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Gene 1.1 ST Array (mogene11st)
Description
Patients with inflammatory lung diseases are often additionally exposed to polycyclic aromatic hydrocarbons like B[a]P and B[a]P-induced alterations in gene expression in these patients may contribute to the development of lung cancer. Mice were intra-nasally treated with lipopolysaccharide (LPS, 20 g/mouse) to induce pulmonary inflammation and subsequently exposed to B[a]P (0.5 mg/mouse) by intratracheal instillation
Publication Title
Altered gene expression profiles in the lungs of benzo[a]pyrene-exposed mice in the presence of lipopolysaccharide-induced pulmonary inflammation.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 32 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Differences between groups of children with obesity and healthy controls.
Publication Title
Looking for new diagnostic tools and biomarkers of hypertension in obese pediatric patients.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus, Homo sapiens
- 63 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HiSeq 2000
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Protein-RNA Networks Regulated by Normal and ALS-Associated Mutant HNRNPA2B1 in the Nervous System.
Sample Metadata Fields
Age, Specimen part, Disease, Cell line, Treatment
View Samples- Homo sapiens
- 41 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
HnRNPA2B1 encodes an RNA binding protein associated with neurodegenerative disorders. However, its function in the nervous system is unclear. Transcriptome-wide cross-linking and immunoprecipitation in mouse spinal cord discover UAGG motifs enriched within ~2,500 hnRNP A2/B1 binding sites and an unexpected role for hnRNP A2/B1 in alternative polyadenylation. Loss of hnRNP A2/B1 results in alternative splicing, including skipping of an exon in amyotrophic lateral sclerosis (ALS)-associated D-amino acid oxidase (DAO) that reduces D-serine metabolism. Inclusion of the DAO exon is also reduced in transgenic ALS mice models. ALS-associated hnRNP A2/B1 D290V mutant patient fibroblasts and motor neurons differentiated from induced pluripotent stem cells demonstrate gain-of-mutant-dependent splicing differences. Mutant motor neurons also exhibit increased hnRNP A2/B1 localization to cytoplasmic granules during stress, which are abrogated by a small molecule CA43. Our findings and cellular resource identify RNA networks affected in loss of normal and mutated hnRNP A2/B1 with broad relevance to neurodegeneration.
Publication Title
Protein-RNA Networks Regulated by Normal and ALS-Associated Mutant HNRNPA2B1 in the Nervous System.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
HnRNPA2B1 encodes an RNA binding protein associated with neurodegenerative disorders. However, its function in the nervous system is unclear. Transcriptome-wide cross-linking and immunoprecipitation in mouse spinal cord discover UAGG motifs enriched within ~2,500 hnRNP A2/B1 binding sites and an unexpected role for hnRNP A2/B1 in alternative polyadenylation. Loss of hnRNP A2/B1 results in alternative splicing, including skipping of an exon in amyotrophic lateral sclerosis (ALS)-associated D-amino acid oxidase (DAO) that reduces D-serine metabolism. Inclusion of the DAO exon is also reduced in transgenic ALS mice models. ALS-associated hnRNP A2/B1 D290V mutant patient fibroblasts and motor neurons differentiated from induced pluripotent stem cells demonstrate gain-of-mutant-dependent splicing differences. Mutant motor neurons also exhibit increased hnRNP A2/B1 localization to cytoplasmic granules during stress, which are abrogated by a small molecule CA43. Our findings and cellular resource identify RNA networks affected in loss of normal and mutated hnRNP A2/B1 with broad relevance to neurodegeneration.
Publication Title
Protein-RNA Networks Regulated by Normal and ALS-Associated Mutant HNRNPA2B1 in the Nervous System.
Sample Metadata Fields
Specimen part, Disease, Treatment
View Samples- Mus musculus
- 7 Downloadable Samples
- Illumina HiSeq 2000
Description
HnRNPA2B1 encodes an RNA binding protein associated with neurodegenerative disorders. However, its function in the nervous system is unclear. Transcriptome-wide cross-linking and immunoprecipitation in mouse spinal cord discover UAGG motifs enriched within ~2,500 hnRNP A2/B1 binding sites and an unexpected role for hnRNP A2/B1 in alternative polyadenylation. Loss of hnRNP A2/B1 results in alternative splicing, including skipping of an exon in amyotrophic lateral sclerosis (ALS)-associated D-amino acid oxidase (DAO) that reduces D-serine metabolism. Inclusion of the DAO exon is also reduced in transgenic ALS mice models. ALS-associated hnRNP A2/B1 D290V mutant patient fibroblasts and motor neurons differentiated from induced pluripotent stem cells demonstrate gain-of-mutant-dependent splicing differences. Mutant motor neurons also exhibit increased hnRNP A2/B1 localization to cytoplasmic granules during stress, which are abrogated by a small molecule CA43. Our findings and cellular resource identify RNA networks affected in loss of normal and mutated hnRNP A2/B1 with broad relevance to neurodegeneration. Overall design: RNA-seq in mouse spinal after injection with ASO against hnRNP A2/B1 or saline. Three or four replicates per condition
Publication Title
Protein-RNA Networks Regulated by Normal and ALS-Associated Mutant HNRNPA2B1 in the Nervous System.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples