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GSE18517
Glycine max
43 Downloadable Samples
Affymetrix Soybean Genome Array (soybean)
Description
Gene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.
Publication Title
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Glycine max
- 24 Downloadable Samples
- Affymetrix Soybean Genome Array (soybean)
Description
Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.
Publication Title
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Glycine max
- 17 Downloadable Samples
- Affymetrix Soybean Genome Array (soybean)
Description
Gene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937).
Publication Title
Identification of Aluminum Responsive Genes in Al-Tolerant Soybean Line PI 416937.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
In this study, we initially screened over 1400 natural products for capacity to inhibit the kinetic enzyme activity of nuclear HDACs isolated from SK-MEL-3 cells. From these findings we evaluate whole transcriptome changes that occur at a 24 hour time point in SK-ME-3 cells in the presence of a known HDAC inhibitor (Trichostatin A) (1uM) or a natural product HDAC inhibitor Grapeseed Extract (120ug/ml), both tested at sub-lethal concentrations relative to untreated controls. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip Human 2.1ST ARRAY by Affymetrix Inc
Publication Title
Whole-transcriptomic Profile of SK-MEL-3 Melanoma Cells Treated with the Histone Deacetylase Inhibitor: Trichostatin A.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Myc is an oncogenic transcription factor frequently dysregulated in human cancer. To identify pathways supporting the Myc oncogenic program, we employed a genome-wide RNAi screen for Myc-synthetic-lethal (MySL) genes and uncovered a role for the SUMO-activating-enzyme (SAE1/2). Loss of SAE1/2 enzymatic activity drives synthetic lethality with Myc. Mechanistically, SAE2 inhibition switches a transcriptional subprogram of Myc from activated to repressed. A subset of these SUMOylation-dependent Myc-switchers (SMS genes) governs mitotic spindle function and is required to support the Myc oncogenic program.
Publication Title
A SUMOylation-dependent transcriptional subprogram is required for Myc-driven tumorigenesis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
The effects of BSE and 3-OABA on MDA-MB-231 cells were evaluated for effects on the whole transcriptome: including mRNAs and long intergenic non-coding RNA transcripts (lincRNA) using GeneChip Human Gene 2.1 ST Arrays by Affymetrix Inc.
Publication Title
Transcriptomic Profiling of MDA-MB-231 Cells Exposed to <i>Boswellia Serrata</i> and 3-O-Acetyl-B-Boswellic Acid; ER/UPR Mediated Programmed Cell Death.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 47 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Levels of C/EBP are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis. To assess the mechanisms involved in these effects, C/EBP targets were identified by microarray analyses. Upon C/EBP activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBP was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBP while c-Myb siRNA treatment enhanced C/EBP-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBP but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBP induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBP activation. In summary, the effects of C/EBP in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2. Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBP appear to involve different transcription-regulated targets.
Publication Title
Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
Illumina humanRef-8 v1.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina humanRef-8 v1.0 expression beadchip
Description
Determine the role of interferons in the transcriptional profile of Ad-F7 transduced primary human macrophages using neutralizing antibody for the type I IFN receptor (IFNAR2).
Publication Title
Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 43 Downloadable Samples
Illumina HiSeq 2000
Description
Longevity mechanisms increase lifespan by counteracting the effects of aging. However, whether longevity mechanisms counteract the effects of aging continually throughout life, or whether they act during specific periods of life, preventing changes that precede mortality is unclear. Here, we uncover transcriptional drift, a phenomenon that describes how aging causes genes within functional groups to change expression in opposing directions. These changes cause a transcriptome-wide loss in mRNA stoichiometry and loss of co-expression patterns in aging animals, as compared to young adults. Using Caenorhabditis elegans as a model, we show that extending lifespan by inhibiting serotonergic signals by the antidepressant mianserin attenuates transcriptional drift, allowing the preservation of a younger transcriptome into an older age. Our data are consistent with a model in which inhibition of serotonergic signals slows age-dependent physiological decline and the associated rise in mortality levels exclusively in young adults, thereby postponing the onset of major mortality. Overall design: In this study set out to measure aging in the transcriptome by determining drift-variance changes with age in C.elegans. We set up three different cohorts of water or mianserin treated animals. The title of each cohort indicates the treatment (e.g. h2o or mia), the concentration (mia2, mia10, mia50), the day when the treatment was started (e.g. d1= day 1 of adulthood) and the day when the sample was collected (e.g. d10= day 10 of adulthood). cohort #1: Celegans was treated with water or mianserin (50uM) on day 1 and RNA was harvested on day1 (water only), d3, d5 and day 10 (file titles: h2o d1/d1, h2o d1/d3, h2o d1/d5, h2o d1/d10, mia50 d1/d3, mia50 d1/d5, mia50 d1/d10) cohort #2: Celegans was treated with mianserin (50uM) starting on day 3, and day 5, RNA was harvested on day 5 or 10 (file titles: mia50 d3/d10, mia50 d5/d10, mia50 d3/d5) cohort #3: Celegans was treated with mianserin 2 uM and 10 uM Mianserin on day 1 and Rna harvested on day 5 (file titles: mia2 d1/d5, mia10 d1/d5)
Publication Title
Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality.
Sample Metadata Fields
Subject
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