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Homo sapiens
24 Downloadable Samples
Illumina HiSeq 2000
Description
The transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs) Overall design: A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)
Publication Title
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Sample Metadata Fields
Treatment, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HiSeq 2000
Description
The transcriptional profile of A673 parental, and SP-2509 drug resistant washout cells (4 and 6 months) Overall design: Following generation of A673 SP-2509 drug resistant cells (chronic exposure for 7 months), drug was withdrawn with cell pellets collected 4 and 6 months after removal.
Publication Title
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Sample Metadata Fields
Disease, Treatment, Subject
View Samples- Homo sapiens
- 36 Downloadable Samples
- Illumina HiSeq 4000
Description
The purpose of this study was to define biomarkers of sensitivty and mechanisms of resistance to the KDM1A/LSD1 inhibtor SP-2509 (HCI-2509) in Ewing sarcoma cell lines. We report that regardless of drug sensitivity all cell lines engage the UPR and ER-stress response following treatment with SP-2509 resulting in apoptotic cytotoxicity. In addition hypersentsitive cell lines shared a common basal transcriptnomic profile, with hypersensitive cell lines signficantly inducing ETS1 which was not observed in sensitive cell lines. Overall design: 6 Ewing sarcoma cell lines were treated with either vehicle control (DMSO) or the reversible LSD1/KDM1A inhibitor SP-2509 (2uM) for 48hrs. Three SP-2509 hypersensitive (IC50< 300nM)(A673, TC32, TC252) and three SP-2509 sensitive (IC50>900nM) (EWS-502, ES-2 and TC71) cell lines were investigated. Paired RNA from three indpendent experiments per cell line was analyzed.
Publication Title
Therapeutic Targeting of KDM1A/LSD1 in Ewing Sarcoma with SP-2509 Engages the Endoplasmic Reticulum Stress Response.
Sample Metadata Fields
Treatment, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This study has examined the molecular mechanisms underlying sensitivity of sarcomas to Nutlin-3a, a non-genotoxic activator of the p53 pathway. Human patient material was collected immediately following surgical resection, dissected into small pieces and ex planted onto gelatin sponges immersed in media containing either vehicle control or Nutlin-3a (10uM and/or 50uM) for 48 hours.
Publication Title
Nutlin-3a efficacy in sarcoma predicted by transcriptomic and epigenetic profiling.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Identification of gene expressed in the enriched inner medullary collecting duct cells in rat.
Publication Title
Transcriptional profiling of native inner medullary collecting duct cells from rat kidney.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
APC mutant mice develop polys in the intestine, but not carcinoma. We found that additional deletion of Olfm4 gene induced carcinoma formation in the distal colon. To explore the molecular mechanism, we performed cDNA microarray to understand the gene expression files in the tumor tissues compared with WT, APC mutant and Olfm4 mutant mice.
Publication Title
Olfactomedin 4 deletion induces colon adenocarcinoma in Apc<sup>Min/+</sup> mice.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
Cohesin, which consists of SMC1, SMC3, Rad21 and either SA1 or SA2, topologically embraces the chromatin fibers to hold sister chromatids together and to stabilize chromatin loops. Increasing evidence indicates that these loops are the organizing principle of higher-order chromatin architecture, which in turn is critical for gene expression. To determine how cohesin contributes to the establishment of tissue-specific transcriptional programs, we compared genome-wide cohesin distribution, gene expression and chromatin architecture in cerebral cortex and pancreas from adult mice. More than one third of cohesin binding sites differ between the two tissues and these are enriched at the regulatory regions of tissue-specific genes. Cohesin colocalizes extensively with the CCCTC-binding factor (CTCF). Cohesin/CTCF sites at active enhancers and promoters contain, at least, cohesin-SA1 whereas either cohesin-SA1 or cohesin-SA2 are present at active promoters independently of CTCF. Analyses of chromatin contacts at the Protocadherin gene cluster and the Regenerating islet-derived (Reg) gene cluster, mostly expressed in brain and pancreas respectively, revealed remarkable differences in the architecture of these loci in the two tissues that correlate with the presence of cohesin. Moreover, we found decreased binding of cohesin and reduced transcription of the Reg genes in the pancreas of SA1 heterozygous mice. Given that Reg proteins are involved in the control of inflammation in pancreas, such reduction may contribute to the increased incidence of pancreatic cancer reported in these animals. Overall design: Examination of the relationship between gene expression, genome wide cohesin distribution and chromatin structure
Publication Title
The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Illumina HiSeq 2000
Description
Changes in gene expression caused by CREBBP/EP300 bromodomain inhibitors in a CML cell line Overall design: K562 cells were treated with CBP30 and I-CBP112 and changes in gene expression were evaluated by RNA-seq
Publication Title
CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples
SRP068961- Homo sapiens
- 8 Downloadable Samples
- IlluminaHiSeq2000
Description
Antiprolifereative effects of CREBBP/EP300 inhibitors were tested in human leukemia and lymphoma cell lines and the molecular mechanisms responsible for such effects were explored. Overall design: K562 cells were treated with CBP-30 (CREBBP/EP300 bromodomain inhibitor), C646 (CREBBP/EP300 HAT activity inhibitor) and JQ1 (BRD4 inhibitor) and changes in gene expression were evaluated by RNA-seq.
Publication Title
CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 2 Downloadable Samples
- Illumina Genome Analyzer II
Description
Purpose: Validation of Drosophila A-to-I editing sites Methods: We collected heads of 5 day old male dAdar-/- mutant (y, Adar5G1, w)26 and wild type (w1118) flies. Poly(A)+ RNA was used to prepare RNA-seq libraries which were subsequently sequenced single-end by an Illumina GAII Results:We builded a framework to identify RNA editing events using RNA-seq data alone in Drosophila. To validate whether the identified A-to-G sites were bona fide A-to-I editing events, we performed RNA-seq for the D.melanogaster wild-type strain (w1118) and for the Adar5G1 null mutant that eliminates RNA editing. We found that our method achieved high accuracy; 98.2% of all A-to-G sites showed only adenosine in the Adar5G1 sample Conclusions: We anticipate that our method will be very effective in the future to identify RNA editing events in different species. Overall design: mRNA profiles of heads of 5 day old male dAdar-/- mutant (y, Adar5G1, w)26 and wild type (w1118) flies
Publication Title
Identifying RNA editing sites using RNA sequencing data alone.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples