Filters
Technology
Platform
GSE60933
Mus musculus
5 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Dual oxidases play a role in innate host defense at barrier epithelia. We examined the effect of loss of dual oxidase function (duoxa-/-) on gene expression in the mouse terminal ileum at homeostasis. To control for cage/litter effects, duoxa-/- were cohoused with wild type littermate controls.
Publication Title
Increased Expression of DUOX2 Is an Epithelial Response to Mucosal Dysbiosis Required for Immune Homeostasis in Mouse Intestine.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC).
Publication Title
Functional Characterization of Inflammatory Bowel Disease-Associated Gut Dysbiosis in Gnotobiotic Mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The pancreatic beta cells are the only cells that can produce insulin in response to prevailing glycemia. The development of beta cells was found to be depending on the activity of a complex genetic network. Overexpression of transcriptional factor MafK in beta cells have resulted in impairment of thier functions and suppressed insulin secretion and increased the severity of beta cell loss resulting in an overt diabetes.
Publication Title
β-Cell-Specific Mafk Overexpression Impairs Pancreatic Endocrine Cell Development.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 66 Downloadable Samples
IlluminaHiSeq1500
Description
The goal of this study is to simultaneously interrogate host and parasite gene expression programs in human macrophages infected with the intracellular parasites from the genus Leishmania. We conducted high-resolution sequencing of the transcriptomes of human macrophages infected with Leishmania spp. using an RNA-seq approach. An array of computational tools was applied to map reads to the Leishmania and human genomes and reconstruct full-length transcripts. mRNA abundance was determined for Leishmania and human genes at various time points post-infection, enabling us to identify co-expression patterns that correlate with the biology of the parasite and to obtain a preliminary analysis of the dynamic nature of parasite and host cell gene expression programs in the context of infection. This study provides a solid framework for future functional and genomic studies of leishmaniasis as well as intracellular pathogenesis in general.
Publication Title
Dual Transcriptome Profiling of Leishmania-Infected Human Macrophages Reveals Distinct Reprogramming Signatures.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 7 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
We conducted a preliminary investigation to determine whether ethanol-induced alterations in placental gene expression may have some utility as a diagnostic indicator of maternal drinking during pregnancy as well as a prognostic indicator of risk for adverse neurobehavioral outcomes in affected offspring.
Publication Title
Effects of moderate drinking during pregnancy on placental gene expression.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 21 Downloadable Samples
- Illumina HiSeq 1500
Description
Macrophages readily change their phenotype in response to exogenous stimuli. In this work, macrophages were stimulated under a variety of experimental conditions, and alterations in mRNA levels were analyzed. We identified three transcriptionally related populations of macrophages with immunoregulatory activity. They were generated by stimulating cells with TLR ligands, in the presence of three different “reprogramming” signals; high density immune complexes (IC), prostaglandin E2 (PGE2), or adenosine (Ado). All three of these cell populations produced higher levels of transcripts for IL-10, and growth and angiogenic factors. They also secreted reduced levels of inflammatory cytokines IL-1Beta, IL-6, and IL-12. All three macrophage phenotypes could partially rescue mice from lethal endotoxemia, and therefore we consider each to have immunoregulatory activity. This immunoregulatory activity occurred equally well in macrophages from stat6-deficient mice. The lack of STAT6 did not affect macrophages’ ability to reciprocally change cytokine production or to rescue mice from lethal endotoxemia. Furthermore, treatment of macrophages with IL-4 failed to induce similar phenotypic or transcriptional alterations. This work demonstrates that there are multiple ways to generate macrophages with immunoregulatory activity. These immunoregulatory macrophages are transcriptionally and functionally related, and quite distinct from macrophages treated with IL-4.
Publication Title
The generation of macrophages with anti-inflammatory activity in the absence of STAT6 signaling.
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- Mus musculus
- 90 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 Liver 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