Filters
Technology
Platform
SRP047000
Drosophila melanogaster
12 Downloadable Samples
Illumina HiSeq 2000
Description
PcG protein complex PRC2 is a methyltransferase specific for histone H3 lysine27, and H3K27me3 is essential for stable transcription silencing. Less well known but quantitatively much more important is the genome-wide role of PRC2 that dimethylates ~70% of total H3K27. Here we show that H3K27me2 occurs in inverse proportion to transcriptional activity in genes and intergenic regions and its loss results in global transcriptional derepression proportionally greatest in previously silent or weakly transcribed regions. H3K27me2 levels are controlled by opposing roaming activities of PRC2 and the H3K27 demethylase dUTX. Unexpectedly, we find an equally pervasive distribution of histone H2A ubiquitylated at lysine 118 (H2AK118ub), attributed to the RING1 subunit of PRC1-type complexes. Overall design: Examination of global changes in transcription genome-wide when E(z) is inactivated by monitoring total RNA from E(z) temperature-sensitive cells at 25°C and 31°C in duplicate
Publication Title
Genome-wide activities of Polycomb complexes control pervasive transcription.
Sample Metadata Fields
Cell line, Subject
View Samples- Drosophila melanogaster
- 18 Downloadable Samples
Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Discovery of progenitor cell signatures by time-series synexpression analysis during Drosophila embryonic cell immortalization.
Sample Metadata Fields
Cell line
View Samples- Drosophila melanogaster
- 32 Downloadable Samples
- Illumina HiSeq 2000
Description
To characterize the sequence of events associated with RasV12 immortalization of Drosophila embryonic cells, we generated transcriptional time series during cell line establishment, from primary cultures until passage (P) 19. Overall design: We generated three transcriptional time series from three cell lines (R1, R4 and R5) by sampling the cultures at successive stages, early (P2-4), intermediate (P4-11), and late (P16-19), characterized by different passage times. Time points for the R1 time-series were: P2, P3, P4, P5, P7, P8, P10, P11, P16, P17 and P19; for the R4 time-series: P2, P3, P4, P5, P6, P7, P9, P11, P12, P16, P17 and P19; and for the R5 time-series: P2, P3, P4, P6, P7, P8, P16, P17 and P19
Publication Title
Discovery of progenitor cell signatures by time-series synexpression analysis during Drosophila embryonic cell immortalization.
Sample Metadata Fields
Cell line, Subject
View Samples- Drosophila melanogaster
- 18 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
To characterize the sequence of events associated with RasV12 immortalization of Drosophila embryonic cells, we generated transcriptional time series during cell line establishment, from primary cultures until passage (P) 19.
Publication Title
Discovery of progenitor cell signatures by time-series synexpression analysis during Drosophila embryonic cell immortalization.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Prolonged cold exposure stimulates the recruitment of beige adipocytes within white adipose tissue. Beige adipocytes depend on mitochondrial oxidative phosphorylation to drive thermogenesis. The transcriptional coregulator TLE3 inhibits mitochondrial and metabolic gene expression in beige adipocytes. Overall design: mRNA profiles of iWAT immortalized preadipocytes, differentiated in culture, and knocking out TLE3 after differentiation, were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500.
Publication Title
Loss of TLE3 promotes the mitochondrial program in beige adipocytes and improves glucose metabolism.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome Array (drosgenome1)
Description
The highly conserved Epidermal Growth Factor-receptor (Egfr) pathway is required in all animals for normal development and homeostasis; consequently, aberrant Egfr signaling is implicated in a number of diseases. Genetic analysis of Drosophila melanogaster Egfr has contributed significantly to understanding this conserved pathway and has led to the discovery of new components and targets. Here we used microarray analysis of Drosophila third instar wing discs, in which Egfr signaling was perturbed, to identify new Egfr-responsive genes. Upregulated transcripts included five known targets suggesting the approach was valid. We investigated the function of 29 previously uncharacterized genes, which had pronounced responses. The Egfr pathway is important for wing-vein patterning and using reverse genetic analysis we identified five genes that showed venation defects. Three of these genes are expressed in vein primordia and all showed transcriptional changes in response to altered Egfr activity consistent with being targets of the pathway. Genetic interactions with Egfr further linked two of the genes, Sulfated (Sulf1), an endosulfatase gene, and CG4096, an ADAMTS (A Disintegrin And Metalloproteinase with ThromboSpondin motifs) gene, to the pathway. Sulf1 showed a strong genetic interaction with the neuregulin-like ligand vein (vn) and may influence binding of Vn to heparan-sulfated proteoglycans (HSPGs). Genetic evidence also shows that CG4096 functions by modulating activity of the Egfr ligands. The substrate(s) and how ligand activity is affected are unknown, but interestingly vertebrate EGF ligands are regulated by a related ADAMTS protein. We conclude Sulf1 and CG4096 are negative feedback regulators of Egfr signaling that function in the extracellular space to influence ligand activity.
Publication Title
New negative feedback regulators of Egfr signaling in Drosophila.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 94 Downloadable Samples
- IlluminaHiSeq2000
Description
We obtained radiographically-localized biopsies during glioma resection surgeries to sample the tumor core and margins from multiple glioma patients. We also procured fresh, non-neoplastic brain tissue specimens from multiple patients having procedures to relieve epilespy symptoms or to place shunts to treat normal pressure hydrocephalus. We then used RNA-Seq to compare expression patterns between geographically distinct regions of gliomas and computational deconvolution to estimate cell type-specific expression patterns in different disease subtypes. Overall design: RNA-Seq analysis in 39 contrast-enhancing glioma core samples, 36 non-enhancing FLAIR glioma margin samples, and 17 non-neoplastic brain tissue samples.
Publication Title
MRI-localized biopsies reveal subtype-specific differences in molecular and cellular composition at the margins of glioblastoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Homo sapiens
- 219 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
RG7212 anti-TWEAK mAb inhibits tumor growth through inhibition of tumor cell proliferation and survival signaling and by enhancing the host antitumor immune response.
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line, Race, Time
View Samples- Homo sapiens
- 59 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tumor necrosis factor-related weak inducer of apoptosis, TWEAK, is a TNF superfamily member that mediates signaling through its receptor fibroblast growth factor inducible-14, Fn14. In tumor cell lines, TWEAK induces proliferation, survival and NF-kappaB signaling and gene expression that promote tumor growth and suppress antitumor immune responses. Anti-TWEAK antibody, RG7212, inhibits tumor growth in vivo with decreases in pathway activation markers and modulation of tumor, blood and spleen immune cell composition. Candidate response prediction markers, including Fn14, have been identified in mouse models. Phase I pharmacodynamic data from patients are consistent with preclinical results. TWEAK:Fn14 signaling is upregulated in human cancer and pathway activation induces tumor proliferation and survival signaling. Blockade with anti-TWEAK mAb, RG7212, inhibits tumor growth in multiple models in mice. TWEAK induces changes that suppress anti-tumor immune responses and RG7212 blocks these effects resulting in changes in tumor immune cell composition and decreases in cytokines that promote immunosuppression. Antitumor efficacy in mice was observed in a range of Fn14 expressing models with pathway activation and expressing either wild-type or mutant p53, BRAF or KRAS suggesting both a patient selection strategy and potential broad clinical applicability. Preclinical mechanism of action hypotheses are supported by Phase I clinical data, with decreases in proliferation markers and increased tumor T cell infiltration.
Publication Title
RG7212 anti-TWEAK mAb inhibits tumor growth through inhibition of tumor cell proliferation and survival signaling and by enhancing the host antitumor immune response.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 49 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tumor necrosis factor-related weak inducer of apoptosis, TWEAK, is a TNF superfamily member that mediates signaling through its receptor fibroblast growth factor inducible-14, Fn14. In tumor cell lines, TWEAK induces proliferation, survival and NF-kappaB signaling and gene expression that promote tumor growth and suppress antitumor immune responses. Anti-TWEAK antibody, RG7212, inhibits tumor growth in vivo with decreases in pathway activation markers and modulation of tumor, blood and spleen immune cell composition. Candidate response prediction markers, including Fn14, have been identified in mouse models. Phase I pharmacodynamic data from patients are consistent with preclinical results. TWEAK:Fn14 signaling is upregulated in human cancer and pathway activation induces tumor proliferation and survival signaling. Blockade with anti-TWEAK mAb, RG7212, inhibits tumor growth in multiple models in mice. TWEAK induces changes that suppress anti-tumor immune responses and RG7212 blocks these effects resulting in changes in tumor immune cell composition and decreases in cytokines that promote immunosuppression. Antitumor efficacy in mice was observed in a range of Fn14 expressing models with pathway activation and expressing either wild-type or mutant p53, BRAF or KRAS suggesting both a patient selection strategy and potential broad clinical applicability. Preclinical mechanism of action hypotheses are supported by Phase I clinical data, with decreases in proliferation markers and increased tumor T cell infiltration.
Publication Title
RG7212 anti-TWEAK mAb inhibits tumor growth through inhibition of tumor cell proliferation and survival signaling and by enhancing the host antitumor immune response.
Sample Metadata Fields
Sex, Disease, Cell line, Race, Time
View Samples