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SRP019249
Saccharomyces cerevisiae
4 Downloadable Samples
Illumina HiSeq 2000, Illumina Genome Analyzer IIx
Description
Data for replicate Drn1-TAP and Dbr1-TAP CLIP-seq experiments to identify RNA-protein interactions Overall design: Drn1-TAP and Dbr1-TAP CLIP-seq
Publication Title
A homolog of lariat-debranching enzyme modulates turnover of branched RNA.
Sample Metadata Fields
Disease, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- IlluminaHiSeq2000
Description
Neuroblastoma cell lines can differentiate upon retinoic acid (RA) treatment, a finding that provided the basis for the clinical use of RA to treat neuroblastoma. However, resistance to RA is often observed, which limits its clinical utility. Using a gain-of-function genetic screen we identify the transcriptional coactivator Mastermind-like 3 (MAML3) as a gene whose ectopic expression confers resistance to RA. We find that MAML3 expression leads to loss of activation of a subset of RA target genes, which hampers RA-induced differentiation. The regulatory DNA elements of this subset of RA target genes show overlap in binding of MAML3 and the retinoic acid receptor, suggesting a role for MAML3 in the regulation of these genes. In addition, MAML3 has RA independent functions, including the activation of IGF1R and downstream AKT signaling via upregulation of IGF2, resulting in increased proliferation. Our results indicate an important role for MAML3 in differentiation and proliferation of neuroblastomas. Overall design: RNA-seq of SK-N-SH control and MAML3 overexpressing (SD3.23) cells, either untreated (UT) or treated with 1 µM RA (RA).
Publication Title
Mastermind-Like 3 Controls Proliferation and Differentiation in Neuroblastoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
Illumina HumanWG-6 v3.0 expression beadchip
Description
We have identified ZNF423 (also known as Ebfaz, OAZ or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. ZNF423 associates with the RAR/RXR nuclear receptor complex and is essential for transactivation in response to retinoids. Down-regulation of ZNF423 expression by RNA interference in neuroblastoma cells results in a growth advantage and resistance to RA-induced differentiation, whereas overexpression of ZNF423 leads to growth inhibition and enhanced differentiation. Futhermore, we show that low ZNF423 expression is associated with poor disease outcome of neuroblastoma patients. To identify the other key pathways regulated by ZNF423 in human neuroblastoma, we expressed elevated levels of ZNF423 in SH-SY5Y cells and performed full genome gene expression analysis in these cells.
Publication Title
ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
To study the senescence gene signatures in the cells, which were genetic SMARCB1 depleted or treated with aurora kinase inhibitors or etoposide, we performed next generation RNA sequencing on these cell, and ''FRIDMAN_SENESCENCE_UP'' geneset was used to determine the enrichment of senescence-related genes. The RNA sequencing results include (1) A375 cells and SMARCB1 depleted counterparts. (2) A549 cells and aurora kinase inhibitor (Alisertib, barasertib or tozasertib) or etoposide treated counterparts. Overall design: RNA seq data of A375_gSMARCB1 + A549_etoposide, Aurora kinases inhibitors treated, to check senescence gene expression signature one replicate of A375 cells parental V.S SMARCB1 KO (by CRISPR) + duplicates of A549 parental V.S etoposide, or 3 indepdent aurora kinase inhibitors (MLN8237/Alisertib, VX680/Tozasertib, AZD1132/Barasertib)
Publication Title
High-Throughput Functional Genetic and Compound Screens Identify Targets for Senescence Induction in Cancer.
Sample Metadata Fields
Disease, Disease stage, Cell line, Subject
View Samples- Mus musculus
- 232 Downloadable Samples
- Illumina HiSeq 2500
Description
We performed Fluidigm C1 single cell sequencing analysis of wild-type and microRNA deficient (Dgcr8 knockout) mouse embryonic stem cells mock treated or transfected with either miR-294 or let-7. Overall design: Wild-type and Dgcr8 knockout cells grown in naïve culture conditions were mock transfected or transfected with miRNA mimics for let-7b or miR-294, single cells were captured on Fluidigm C1 24 hours post-transfection and then prepared for sequencing on Illumina HiSeq1000 following manufacturer''s protocol.
Publication Title
The impact of microRNAs on transcriptional heterogeneity and gene co-expression across single embryonic stem cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- 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- Mus musculus
- 28 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 13 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Genome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Publication Title
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Genome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Publication Title
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
Sample Metadata Fields
No sample metadata fields
View Samples