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Arabidopsis thaliana
1 Downloadable Sample
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 1 Downloadable Sample
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Utilizing Affymetrix ATH1 microarrays to analyze transposon expression in DNA methylation mutants, and RNAi mutants, compared to wildtype.
Publication Title
miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.
Sample Metadata Fields
Specimen part
View Samples- Oryza sativa
- 12 Downloadable Samples
- Affymetrix Rice Genome Array (rice)
Description
Transgenic rice plants expressing isopentenyltransferase (IPT), an enzyme that catalyzes the rate-limiting step in CK synthesis under the control of SARK, a maturation- and stress-inducible promoter. Increased CK production resulted in sink source alteration and enhanced drought tolerance of the transgenic plants.
Publication Title
Cytokinin-mediated source/sink modifications improve drought tolerance and increase grain yield in rice under water-stress.
Sample Metadata Fields
Age, Specimen part
View Samples
GSE75789- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Glioblastoma multiforme (GBM) is the most aggressive form of brain tumors. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to such treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and -5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased of cell proliferation, and increased cell cycle arrest and apoptosis in comparison to only irradiated cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation and cell cycle regulation. To our knowledge, this is the first study to describe role of miR-338-5p in GBM and its potential to improve sensitivity of GBM to radiation.
Publication Title
MiR-338-5p sensitizes glioblastoma cells to radiation through regulation of genes involved in DNA damage response.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
The murine thymus produces discrete T cell subsets making either IFN- or IL-17, but the role of the TCR in this developmental process remains controversial. Here we generated a non-transgenic and polyclonal model of reduced TCR expression and signal strength selectively on T cells. Mice haploinsufficient for both CD3 and CD3 (CD3DH) showed normal thymocyte subsets but specific defects in T cell development, namely impaired differentiation of IL-17-producing embryonic V6+ (but not adult V4+) T cells and a marked depletion of IFN--producing CD122+ NK1.1+ (V1-biased) T cells throughout life. As result, adult CD3DH mice showed defective peripheral IFN- responses and were resistant to experimental cerebral malaria. Thus, strong TCR signaling is required within specific developmental windows with distinct V usage and differential cytokine production by effector T cell subsets.
Publication Title
TCR signal strength controls thymic differentiation of discrete proinflammatory γδ T cell subsets.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 45 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Barrett's esophagus is characterized by the replacement of squamous epithelium with specialized intestinal metaplastic mucosa. The exact mechanisms of initiation and development of Barrett's metaplasia remain unknown, but a hypothesis of successful adaptation against noxious reflux components has been proposed. To search for the repertoire of adaptation mechanisms of Barrett's metaplasia, we employed high-throughput functional genomic and proteomic methods that defined the molecular background of metaplastic mucosa resistance to reflux. Transcriptional profiling was established for 23 pairs of esophageal squamous epithelium and Barrett's metaplasia tissue samples using Affymetrix U133A 2.0 GeneChips and validated by quantitative real-time polymerase chain reaction. Differences in protein composition were assessed by electrophoretic and mass-spectrometry-based methods. Among 2,822 genes differentially expressed between Barrett's metaplasia and squamous epithelium, we observed significantly overexpressed metaplastic mucosa genes that encode cytokines and growth factors, constituents of extracellular matrix, basement membrane and tight junctions, and proteins involved in prostaglandin and phosphoinositol metabolism, nitric oxide production, and bioenergetics. Their expression likely reflects defense and repair responses of metaplastic mucosa, whereas overexpression of genes encoding heat shock proteins and several protein kinases in squamous epithelium may reflect lower resistance of normal esophageal epithelium than Barrett's metaplasia to reflux components. Despite the methodological and interpretative difficulties in data analyses discussed in this paper, our studies confirm that Barrett's metaplasia may be regarded as a specific microevolution allowing for accumulation of mucosal morphological and physiological changes that better protect against reflux injury.
Publication Title
Molecular defense mechanisms of Barrett's metaplasia estimated by an integrative genomics.
Sample Metadata Fields
Sex, Age
View Samples SRP075376- Homo sapiens
- 12 Downloadable Samples
Illumina HiSeq 2000
Description
Paired-end sequencing of Vector and H-Ras expressing cell lines: p53-del and WT-p53 We found that activated forms of H-Ras and PIK3CA oncogene lead to repression of p63, a p53 family member. They also lead to induction of EMT, a cancer-related process. Our results suggest that, through Ras regulation of p63, this oncogene can drive mammary epithelial cells towards greater invasive ability. Overall design: 4 samples analyzed with 3 replicates each, control samples for each H-Ras line are the Vector cell line created at the same time
Publication Title
Repression of p63 and induction of EMT by mutant Ras in mammary epithelial cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina HiSeq 2500
Description
The Igf2 mRNA binding protein2/Imp2 was selectively deleted from adult mouse muscle; two phenotypes were observed: modestly decreased accrual of skeletal muscle mass after weaning and reduced wheel running activity but normal forced treadmill performance. Reduced voluntary activity occurs when fed a high fat diet but is normalized when consuming standard chow. The reduced muscle mass is due to diminished autocrine Igf2 production, reduced Akt1 activation, disinhibition of Gsk3a and reduced protein synthesis, without altered mTOR complex1 activity. The diet-dependent reduction in spontaneous exercise is accompanied by suboptimal muscle fatty acid oxidation, caused by reduced PPARa mRNA and protein, the former an Imp2 client. Nevertheless, in contrast to global Imp2 deficiency, muscle specific Imp2 inactivation does not alter glucose tolerance or the hypoglycemic effect of insulin. Imp2 deficiency in skeletal muscle reduces autocrine production of Igf2 and fiber growth and disorders nutrient metabolism so as to reduce voluntary physical activity. Overall design: The function of IMP2 in adult muscle has been investigated by creating the IMP2 muscle specific knockout mice. The metabolism of these mice at the whole body level, cellular lever, molecular level have been studied.
Publication Title
IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 79 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent).
Publication Title
Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Treatment, Subject
View Samples- Homo sapiens
- 7 Downloadable Samples
- IlluminaHiSeq2000
Description
We applied ribosome profiling and RNA sequencing to examine gene expression regulation during oncogenic cell transformation. One model involves normal mammary epithelial cells (MCF10A) containing ER-Src. Treatment of such cells with tamoxifen rapidly induces Src, thereby making it possible to kinetically follow the transition between normal and transformed cells. The other model consists of three isogenic cell lines derived from primary fibroblasts in a serial manner (Hahn et al., 1999). EH cell is immortalized by overexpression of telomerase (hTERT), and exhibits normal fibroblast morphology. EL cell expresses hTERT along with both large and small T antigens of Simian virus 40, and it displays an altered morphology but is not transformed. ELR cell expresses hTERT, T antigens, and an oncogenic derivative of Ras (H-RasV12). Overall design: Ribosome profiling and RNA sequencing in two cancer cell models
Publication Title
Many lncRNAs, 5'UTRs, and pseudogenes are translated and some are likely to express functional proteins.
Sample Metadata Fields
No sample metadata fields
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