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GSE30531
Homo sapiens
30 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Microarrays were used to determine the change in gene expression of genes involved in the CDT1/NAE pathway
Publication Title
Quantitative proteomic analysis of cellular protein modulation upon inhibition of the NEDD8-activating enzyme by MLN4924.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MYC regulation of a "poor-prognosis" metastatic cancer cell state.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Expression data from ERBB2 over-expression and EGF stimulation in MCF10A cells
Publication Title
MYC regulation of a "poor-prognosis" metastatic cancer cell state.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Expression data from DHT stimulation vs. control in LNCaP cells
Publication Title
MYC regulation of a "poor-prognosis" metastatic cancer cell state.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
We used microarrays to identify genes that are differentially expressed in the absence of miR-998 expression.
Publication Title
An intronic microRNA links Rb/E2F and EGFR signaling.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 30 Downloadable Samples
Illumina HiSeq 2000
Description
Small ubiquitin-like modifier (SUMO) family proteins regulate target protein functions by post-translational modification. However, a potent and selective inhibitor to target the SUMO pathway has been lacking. Here we describe ML-792, the first mechanism-based SUMO-activating enzyme (SAE) inhibitor with nanomolar potency in cellular assays. ML-792 selectively blocks SAE enzyme activity and total SUMOylation, which leads to reduced cancer cell proliferation. Moreover, induction of the MYC oncogene increased the ML-792 mediated viability effect in cancer cells, indicating potential application of SAE inhibitors in MYC-amplified tumors. Using ML-792, we further explored the critical roles of SUMOylation in mitotic progression and chromosome segregation. Furthermore, expression of an SAE catalytic subunit (UBA2) mutant S95N/M97T rescued SUMOylation loss and the mitotic defect induced by ML-792, confirming the selectivity of ML-792. As a potent and selective SAE inhibitor, ML-792 provides rapid loss of endogenously SUMOylated proteins allowing for novel insights into SUMO biology. Overall design: RNA-SEQ was used to analyze changes in mRNA profiles of human colon and breast cancer cells treated with ML00754792 SAEi
Publication Title
Probing the roles of SUMOylation in cancer cell biology by using a selective SAE inhibitor.
Sample Metadata Fields
Cell line, Treatment, Subject, Time
View Samples- Caenorhabditis elegans
- 27 Downloadable Samples
- Illumina HiSeq 2500
Description
A-to-I RNA editing is a conserved and widespread phenomenon in which adenosine (A) is converted to inosine (I) by adenosine deaminases (ADARs) in double-stranded RNA regions. Although human RNAs contain millions of A-to-I editing sites, most of these occur in noncoding regions and their function is unknown. Knockdown of ADAR enzymes in C. elegans causes defects in normal development but is not lethal as it is in human and mouse, making C. elegans an ideal organism for studying the regulatory effects of RNA editing on the transcriptome. Previous studies in C. elegans indicated competition between RNA interference (RNAi) and RNA editing mechanisms, with the observation that lack of both mechanisms can suppress defects observed when only RNA editing is absent. To study the effects of RNA editing on gene expression and function, we established a novel screen that enabled to identify thousands of RNA editing sites in non-repetitive regions in the genome. These include dozens genes that are edited at their 3’UTR region. We found that these genes are mainly germline and neuronal genes and that they are downregulated in the absence of ADAR enzymes. Moreover, we discovered that almost half of these genes are edited in a developmental-specific manner. In addition, we found that many pseudogenes and other lncRNAs are also extensively downregulated in the absence of ADARs in embryo but not L4 larva developmental stage, while this downregulation is not observed in additional knockout of RNAi. Taken together, our results suggest a role for RNA editing in normal growth and development by regulating silencing via RNAi. Overall design: RNA-seq samples were generated from: 1. wildtype (N2) at embryo stage 2. wildtype (N2) at L4 stage 3. ADAR mutant (BB21 or BB4) worms at L4 stage 4. ADAR mutant (BB21 or BB4) worms at embryo stage 5. ADAR mutant and RNAi mutant (BB23, BB24) at embryo stage RNA in high and low molecular weight fractions was extracted by mirVana kit (ambion). mRNA was sequenced from the high molecular weight fraction by means of Illumina TruSeq® RNA Sample Preparation kit automated by Agilent Bravo Automated Liquid Handling Platform. The resulting libraries were sequences with an Illumina HiSeq 2500.
Publication Title
A-to-I RNA editing promotes developmental stage-specific gene and lncRNA expression.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2500
Description
To uncover genes regulated by mTORC1 and estradiol in uterine Tsc2-null LAM like cells, we performed RNAseq on uteri from 12-week old wild-type (WT) and uterine-specific Tsc2-null (KO) mice that were either untreated (intact), oopherectomized (ovx) or oopherectomized + treated with 17ß-estradiol pellets (E2) for 8 weeks. We identified genes that were both estradiol- and TSC2-mediated. Overall design: Uterine mRNA profiles of 12 week old wild type (WT) and uterine-specific Tsc2-null (KO) mice in the presence or absence of estradiol were generated using Illumina HiSeq2500
Publication Title
Estrogen maintains myometrial tumors in a lymphangioleiomyomatosis model.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Sickle cell disease (SCD) results from a point mutation in the ß-globin gene forming hemoglobin S (HbS), which polymerizes in deoxygenated erythrocytes, triggering recurrent painful vaso-occlusive crises and chronic hemolytic anemia. Reactivation of fetal Hb (HbF) expression ameliorates these symptoms of SCD. Nuclear factor (erythroid derived-2)–like 2 (Nrf2) is a transcription factor that triggers cytoprotective and antioxidant pathways to limit oxidative damage and inflammation and increases HbF synthesis in CD34+ stem cell–derived erythroid progenitors. We investigated the ability of dimethyl fumarate (DMF), a small-molecule Nrf2 agonist, to activate ?-globin transcription and enhance HbF in tissue culture, murine and primate models. DMF recruited Nrf2 to the ?-globin promoters and the locus control region of the ß-globin locus in erythroleukemia cells, elevated HbF in SCD donor–derived erythroid progenitors, and reduced hypoxia-induced sickling. Chronic DMF administration in SCD mice induced HbF and increased Nrf2-dependent genes to detoxify heme and limit inflammation. This improved hematological parameters, reduced plasma-free Hb, and attenuated inflammatory markers. Chronic DMF administration to nonanemic primates increased ?-globin mRNA in BM and HbF protein in red cells. DMF represents a potential therapy for SCD to induce HbF and augment vasoprotection and heme detoxification Overall design: RNA-Seq of 30 samples
Publication Title
Dimethyl fumarate increases fetal hemoglobin, provides heme detoxification, and corrects anemia in sickle cell disease.
Sample Metadata Fields
Age, Specimen part, Treatment, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Gene expression array analysis component. Ligand-dependent transcription by the nuclear receptor glucocorticoid receptor (GR) is mediated by interactions with co-regulators. The role of these interactions in determining selective binding of GR to regulatory elements remains unclear. Recent findings indicate a large fraction of genomic GR binding coincides with chromatin that is accessible prior to hormone treatment, suggesting that receptor binding is dictated by proteins that maintain chromatin in an open state. Combining nucleolytic cleavage and chromatin immunoprecipitation with high-throughput sequencing, we identify the activator protein 1 (AP1) as a major partner for productive GR-chromatin interactions. AP1 is critical for GR-regulated transcription and recruitment to co-occupied regulatory elements, illustrating an extensive AP1-GR interaction network. Importantly, the maintenance of baseline chromatin accessibility facilitates GR recruitment and is dependent on AP1 binding. We propose a model where the basal occupancy of transcription factors act to prime chromatin and direct inducible transcription factors to select regions in the genome.
Publication Title
Transcription factor AP1 potentiates chromatin accessibility and glucocorticoid receptor binding.
Sample Metadata Fields
Sex, Cell line, Treatment, Time
View Samples