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GSE71062
Mus musculus, Homo sapiens
4 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 2 Downloadable Samples
- Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Amplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Publication Title
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 2 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Amplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Publication Title
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Sample Metadata Fields
Cell line, Treatment
View Samples- Oryza sativa, Arabidopsis thaliana
- 16 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
In this study, we used a cross-species network approach to uncover nitrogen (N)-regulated network modules conserved across a model and a crop species. By translating gene network knowledge from the data-rich model Arabidopsis (Arabidopsis thaliana, ecotype Columbia-0) to a crop, rice (Oryza sativa spp. japonica (Nipponbare)), we identified evolutionarily conserved N-regulatory modules as targets for translational studies to improve N use efficiency in transgenic plants.
Publication Title
Cross-Species Network Analysis Uncovers Conserved Nitrogen-Regulated Network Modules in Rice.
Sample Metadata Fields
Age, Specimen part
View Samples- Arabidopsis thaliana
- 23 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Nitrogen and light are two major regulators of plant metabolism and development. While genes involved in the control of each of these signals have begun to be identified, regulators that integrate gene responses to nitrogen and light signals have yet to be determined.
Publication Title
Modeling the global effect of the basic-leucine zipper transcription factor 1 (bZIP1) on nitrogen and light regulation in Arabidopsis.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 24 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Histone methylation modulates gene expression in response to external and internal cues. We uncovered a non-redundant role for the Arabidopsis histone methyltransferase, SDG8, which provides a unique opportunity to study the global function of a specific histone methyltransferase within in a multicellular organism. We previously used a promoter responsive to light and carbon in a positive genetic screen to identify an Arabidopsis carbon and light insensitive mutant cli186. In this study, we characterize the mutant cli186 as a complete deletion of a histone methyltransferase gene SDG8 (now renamed sdg8-5). To assess the global role of SDG8, we compared the global histone methylation patterns and the transcriptome of sdg8-5 to wild type (WT) in the context of a transient carbon and light treatment. We showed that the complete deletion of SDG8 in sdg8-5 is associated with a dramatic reduction of H3K36me3 towards the 3 of the gene body, which correlates with significant reduction in gene expression. We uncovered 1,084 high confidence functional targets of SDG8 affected in both H3K36me3 marks and gene expression that are associated with specific biological processes including defense, photosynthesis, nutrient metabolism and energy metabolism. Importantly, 71% of these functional targets are responsive to carbon and/or light. Our model suggests that SDG8 functions to mark specific sets of genes with H3K36me3 in the gene body for active transcription, to tune genes involved in primary metabolism that are responsive to the energy level in the environment.
Publication Title
The histone methyltransferase SDG8 mediates the epigenetic modification of light and carbon responsive genes in plants.
Sample Metadata Fields
Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
Illumina Genome Analyzer IIx
Description
The goal of this study was to investigate the role of intragenic CTCF in alternative pre-mRNA splicing through a combined CTCF-ChIP-seq and RNA-seq approach. CTCF depletion led to decreased inclusion of weak upstream exons. Overall design: CTCF ChIP-seq was performed in BJAB and BL41 B cell lines and normalized relative to Rabbit Ig control IP-seq reads. RNA-seq was performed in BJAB and BL41 cells transduced with shRNA against CTCF or RFP as a control, and in untransduced cells as well.
Publication Title
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
We have determined that verticillin A is a histone methyltransfease inhibitor that selectively inhibits human SUV39H1, SUV39H2, G9a and GLP to inhibit H3K9 methylation in human colon cancer cells. The objective here is to identify verticillin A target genes in human colon cancer cells.
Publication Title
H3K9 Trimethylation Silences Fas Expression To Confer Colon Carcinoma Immune Escape and 5-Fluorouracil Chemoresistance.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Silymarin (SM) is a popular botanical medicine with purported liver protective effects. SM displays multiple effects in animal models and in cell culture including prevention of liver disease, reduction of inflammation, oxidative stress, and proliferation. Despite a plethora of data indicating that SM impinges on multiple cellular signaling pathways important in inflammation and disease, no unifying mechanisms have been forwarded. To define how SM elicits so many biological effects, the current study presents the first comprehensive transcriptional profiling study of human hepatoma cells treated with SM. The intention of the study was to focus on the early transcriptional events that are associated with SM-induced inhibition of proliferation and inflammation. Collectively, the data demonstrate that SM causes a rapid transcriptional reprogramming of cells that initially manifests as energy stress and slowing of cellular metabolism, leading to inhibition of cell growth and inflammation.
Publication Title
Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Time
View Samples- Homo sapiens
- 40 Downloadable Samples
- Illumina HiSeq 2000
Description
We studied changes in a whole transcriptome during dsDNA virus infection. Overall design: Fibroblasts (MRC5 & HFF) and epithelial cells (ARPE19) were infected with HCMV, HSV1 or Ad5 and total RNA was isolated at 48, 9, or 24 hpi, respectively. Total 15 treatments were used. There were 2 biological replicates analyzed per each treatment.
Publication Title
A tumor-specific endogenous repetitive element is induced by herpesviruses.
Sample Metadata Fields
Specimen part, Subject
View Samples