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Mus musculus, Rattus norvegicus
11 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
A series contains a set of transcript intensity values measured by Affymetrix microarray.
Publication Title
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sample Metadata Fields
Sex, Specimen part
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GSE13667- Mus musculus
- 5 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This series of microarray data contain transcript intensity of mpkCCD cells.
Publication Title
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Freshly isolated rat kidney proximal tubules were subjected for transcript profiling.
Publication Title
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sample Metadata Fields
Sex, Specimen part
View Samples- Rattus norvegicus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Freshly isolated rat kidney medullary thick ascending limbs were subjected for transcript profiling.
Publication Title
Systems-level analysis of cell-specific AQP2 gene expression in renal collecting duct.
Sample Metadata Fields
Sex, Specimen part
View Samples- Rattus norvegicus
- 74 Downloadable Samples
Illumina HiSeq 3000
Description
Purpose: Lithium salts, used for treatment of bipolar disorder, frequently induce nephrogenic diabetes insipidus (NDI), limiting therapeutic success. NDI is associated with loss of expression of the molecular water channel, aquaporin-2, in the renal collecting duct (CD). Here, we use the methods of systems biology in a well-established rat model of lithium-induced NDI to identify signaling pathways activated at the onset of polyuria. Methods: We carried out RNA-sequencing in cortical CDs microdissected from rats treated with lithium for 12-72 hours (vs. time controls). Administration of anti-inflammatory doses of dexamethasone to lithium-treated rats countered the loss of aquaporin-2 protein. Protein mass spectrometry in microdissected cortical CDs provided corroborative evidence, but also identified decreased abundance of several anti-oxidant proteins. Cortical thick ascending limbs of Henle were also microdissected for RNA-Seq at 72 hrs. We carried out RNA-Seq for 2-3 CCD sample per rat (1 lithium-treated rat versus 1 control at 12, 24, 36 hrs). Results and conclusion: Integration of new data with prior data about lithium effects at a molecular level leads to a signaling model in which lithium increases ERK activation leading to induction of NF-?B signaling and an inflammatory-like response that represses Aqp2 gene transcription. Overall design: We carried out RNA-sequencing and protein mass spectrometry in cortical CDs microdissected from rats treated with lithium. We identified signaling pathways that initiate Lithium-induced NDI using systems biology approaches.
Publication Title
RNA-Seq and protein mass spectrometry in microdissected kidney tubules reveal signaling processes initiating lithium-induced nephrogenic diabetes insipidus.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject, Time
View Samples- Drosophila melanogaster
- 18 Downloadable Samples
- Drosophila Gene 1.1 ST Array (drogene11st)
Description
Ectopic expression of DNMT3L in Drosophila causes melanotic tumor in the transgenic flies from fifth generation onwards.
Publication Title
DNMT3L enables accumulation and inheritance of epimutations in transgenic Drosophila.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
CD24 is a potential oncogene reported to be overexpressed in a large variety of human malignancies. We have shown that CD24 is overexpressed in 90% of colorectal tumors at a fairly early stage in the multistep process of carcinogenesis. Anti-CD24 monoclonal antibodies (mAb) induce a significant growth inhibition in colorectal and pancreatic cancer cell lines that express the protein. This study is designed to investigate further the effects of CD24 down-regulation using mAb or small interfering RNA in vitro and in vivo. Western blot analysis showed that anti-CD24 mAb induced CD24 protein down-regulation through lysosomal degradation. mAb augmented growth inhibition in combination with five classic chemotherapies. Xenograft models in vivo showed that tumor growth was significantly reduced in mAb-treated mice. Similarly, stable growth inhibition of cancer cell lines was achieved by down-regulation of CD24 expression using short hairpin RNA (shRNA). The produced clones proliferated more slowly, reached lower saturation densities, and showed impaired motility. Most importantly, down-regulation of CD24 retarded tumorigenicity of human cancer cell lines in nude mice. Microarray analysis revealed a similar pattern of gene expression alterations when cells were subjected to anti-CD24 mAb or shRNA. Genes in the Ras pathway, mitogenactivated protein kinase, or BCL-2 family and others of oncogenic association were frequently down-regulated. As a putative new oncogene that is overexpressed in gastrointestinal malignancies early in the carcinogenesis process, CD24 is a potential target for early intervention in the prevention and treatment of cancer.
Publication Title
Targeting CD24 for treatment of colorectal and pancreatic cancer by monoclonal antibodies or small interfering RNA.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 15 Downloadable Samples
- NextSeq 500
Description
Tumors have the capacity to trigger the formation of blood vessels allowing them to spread to other body parts. We examined here the stem cells that form arteries and veins within tumors and propose that their inhibition reduces metastatic spread. Overall design: Examination of dynamics and differentiation of tissue resident endothelial hierarchy in a melanoma setting
Publication Title
Endovascular progenitors infiltrate melanomas and differentiate towards a variety of vascular beds promoting tumor metastasis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 24 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: Identification of relevant genetic pathways that are altered with aging knowing that the precursors for bone-forming osteoblasts reside in the mesenchymal cell population of bone marrow. Method: harvested and characterized, without in vitro culture, mesenchymal cells form human bone marrow capable of osteogenic differentiation Results: Identification of differentially regulated genes with aging in a highly enriched human bone marrow mesenchymal cell population. Conclusions: we have for the first time identified age-related differential gene expression and DNA methylation patterns in a highly enriched human bone marrow mesenchymal cell populationprofiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions. Overall design: Examination of gene expression and DNA methylation patterns from a highly enriched bone marrow mesenchymal cell population from young (mean age, 28.7 years) versus old (mean age, 73.3 years) women
Publication Title
Global transcriptional profiling using RNA sequencing and DNA methylation patterns in highly enriched mesenchymal cells from young versus elderly women.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 146 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
Dietary gluten proteins (prolamins) from wheat, rye, and barley are the driving forces behind celiac disease, an organ-specific autoimmune disorder that targets both the small intestine and organs outside the gut. In the small intestine, gluten induces inflammation and a typical morphological change of villous atrophy and crypt hyperplasia. Gut lesions improve and heal when gluten is excluded from the diet and the disease relapses when patients consume gluten. Oral immune tolerance towards gluten may be kept for years or decades before breaking tolerance in genetically susceptible individuals. Celiac disease provides a unique opportunity to study autoimmunity and the transition in immune cells as gluten breaks oral tolerance. Seventy-three celiac disease patients on a long-term gluten-free diet ingested a known amount of gluten daily for six weeks. A peripheral blood sample and intestinal biopsies were taken before and six weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus height to crypt depth ratio to quantify gluten-induced gut mucosal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained or broke oral tolerance in the face of a gluten challenge.
Publication Title
A B-Cell Gene Signature Correlates With the Extent of Gluten-Induced Intestinal Injury in Celiac Disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment, Subject
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