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GSE19641
Mus musculus
2 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Sandhoff disease (SD) is a lysosomal storage disorder characterized by the absence of -hexosaminidase and storage of GM2 ganglioside and related glycolipids. We found the alterations in the thymus during the development of mild to severe progressive neurologic disease.
Publication Title
No associated publication
Sample Metadata Fields
Age, Specimen part
View Samples- Arabidopsis thaliana
- 72 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Arabidopsis seedlings of the wild-type or hormone mutants were treated with plant hormones.
Publication Title
The AtGenExpress hormone and chemical treatment data set: experimental design, data evaluation, model data analysis and data access.
Sample Metadata Fields
Treatment, Time
View Samples- Arabidopsis thaliana
- 60 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Arabidopsis seedlings of the wild-type were treated with inhibitors.
Publication Title
The AtGenExpress hormone and chemical treatment data set: experimental design, data evaluation, model data analysis and data access.
Sample Metadata Fields
Treatment, Time
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Arabidopsis Gene 1.1 ST Array (aragene11st)
Description
7-days-old Arabidopsis seedlings of wildtype (Col-0) were treated with 1 M IAA for 15 minutes or 3 hours and gene expression of whole plant was analyzed using Affymetrix Gene 1.1 ST Array strips.
Publication Title
AtCAST3.0 update: a web-based tool for analysis of transcriptome data by searching similarities in gene expression profiles.
Sample Metadata Fields
Age, Treatment, Time
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Arabidopsis seedlings of wildtype or ire1a ire1b double mutant were treated with or without tunicamycine in the presence of actinomycin D (ActD).
Publication Title
Defects in IRE1 enhance cell death and fail to degrade mRNAs encoding secretory pathway proteins in the Arabidopsis unfolded protein response.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
MafB is a member of the Maf family of bZip transcription factor and plays important roles in the developmental processes of various tissues, as well as in cell-type specific gene expression. MafB is expressed in differentiating keratinocytes in mice and is transcriptionally up-regulated upon human keratinocyte differentiation in vitro. In MafB-deficient mice, epidermal differentiation is partially impaired and the cornified layer is thinner. To gain insights into more detailed molecular mechanisms of MafB regulation of epidermal development, we performed microarray analysis of mRNAs isolated from dorsal skin epidermis of MafB-/- and wild-type mice at E18.5.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear.
Publication Title
Comprehensive Screening of Gene Function and Networks by DNA Microarray Analysis in Japanese Patients with Idiopathic Portal Hypertension.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have previously shown that during lactation, osteocytes directly remodel their perilacunar and pericanalicular matrix, thereby mobilizing calcium and contributing to maternal bone loss. To identify genes potentially responsible for perilacunar remodeling, microarray analysis was performed on osteocytes from CD-1 virgin and lactating mice and mice sacrificed on day 7 post weaning.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 38 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). The control group was only used in the primary and secondary BMT assays, whereas the three leukemic groups including AE9a, AE9a+miR-126 and miR-126KO+AE9a were used in four passages (i.e., primary, secondary, tertiary and quaternary) of BMT assays. Then, gene expression profiling was conducted with bone marrow samples collected from different groups to decipher the molecular mechanisms underlying miR-126 effects on leukemia initiation and progression and maintenance and self-renewal of leukemia stem/initiating cells.
Publication Title
Overexpression and knockout of miR-126 both promote leukemogenesis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Melanoma is the deadliest form of skin cancer with rising incidence and mortality rates. Oncogenic mutation in BRAF gene is the single most frequent genetic alteration in human melanoma; however, this event per se is not sufficient to produce melanoma in vivo. We have investigated whether epigenetic changes, specifically aberrant DNA methylation and dysregulation of gene expression, alone or in combination with this genetic event, are involved in the genesis of human melanoma. We have constructed the whole of primary human melanomas in relation to their BRAF mutational status. Our methylation profiling identified a large number of hyper- or hypomethylated genes in melanoma tumors, many of which being novel and having the potential to serve as biomarkers. Gene ontology analysis revealed that gene categories involved in neuronal cell morphology and development, and skin and neurological disorders were highly enriched. Frequently methylated targets included developmental regulatory transcription factors and homeobox genes, which are mostly subjected to bivalent histone marking and Polycomb occupancy in embryonic stem cells. Notably, several genes involved in the MEK-ERK and the PI3K pathways, two of the most frequently perturbed pathways in human melanoma, showed extensive methylation changes. Gene expression profiling identified a long list of dysregulated genes, many of which being involved in melanocytes development and differentiation, and showing concomitant aberrant DNA methylation. Sub-typing of the melanoma tumors based on BRAF mutational status revealed that tumors with a mutated BRAF had distinctive and more pronounced changes in both DNA methylation and gene expression profiles than tumors carrying the wildtype BRAF. The differentially compromised methylome and transcriptome of melanomas (dependent on BRAF mutation) deserves special attention because many epigenetic alterations, including DNA methylation-mediated regulation of gene expression, are potentially reversible. The dichotomous integrity of epigenome in human melanoma holds great promise for the field of personalized medicine.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Disease
View Samples