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accession-icon GSE49590
Expression data from 10 day old Arabidopsis thaliana seedlings
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Microarrays were used to detail the global programme of gene expression comparing wild-type and RNAi knock-down plants of SPT4-1 and SPT4-2

Publication Title

The transcript elongation factor SPT4/SPT5 is involved in auxin-related gene expression in Arabidopsis.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE41802
Isocitrata Dehydrogenase (IDH) Mutations Promote a Reversible ZEB1/mir-200-Dependent Epithelial Mesenchymal Transition (EMT)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis

Publication Title

Isocitrate dehydrogenase (IDH) mutations promote a reversible ZEB1/microRNA (miR)-200-dependent epithelial-mesenchymal transition (EMT).

Sample Metadata Fields

Cell line

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accession-icon SRP076716
Three different in vivo models of synovial sarcoma (xenograft: Fuji; PDX: CTG-0331 and CTG-0771) treated with or without the indicated dose of the EZH2 inhibitor, tazemetostat
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The catalytic activities of covalent and ATP-dependent chromatin remodeling are central to regulating the conformational state of chromatin and the resultant transcriptional output. The enzymes that catalyze these activities are often contained within multiprotein complexes in nature. Two such multiprotein complexes, the polycomb repressive complex 2 (PRC2) methyltransferase and the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeler have been reported to act in opposition to each other during development and homeostasis. An imbalance in their activities induced by mutations/deletions in complex members (e.g. SMARCB1) has been suggested to be a pathogenic mechanism in certain human cancers. Here we show that preclinical models of synovial sarcoma - a cancer characterized by functional SMARCB1 loss via its displacement from the SWI/SNF complex through the pathognomonic SS18-SSX fusion protein - display sensitivity to pharmacologic inhibition of EZH2, the catalytic subunit of PRC2. Treatment with tazemetostat, a clinical-stage, selective and orally bioavailable small-molecule inhibitor of EZH2 enzymatic activity reverses a subset of synovial sarcoma gene expression and results in concentration-dependent cell growth inhibition and cell death specifically in SS18-SSX fusion-positive cells in vitro. Treatment of mice bearing either a cell line or two patient-derived xenograft models of synovial sarcoma leads to dose-dependent tumor growth inhibition with correlative inhibition of trimethylation levels of the EZH2-specific substrate, lysine 27 on histone H3. These data demonstrate a dependency of SS18-SSX-positive, SMARCB1-deficient synovial sarcomas on EZH2 enzymatic activity and suggests the potential utility of EZH2-targeted drugs in these genetically defined cancers. Overall design: Three different in vivo models of synovial sarcoma (xenograft: Fuji; PDX: CTG-0331 and CTG-0771) treated with or without the indicated dose of the EZH2 inhibitor, tazemetostat

Publication Title

Preclinical Evidence of Anti-Tumor Activity Induced by EZH2 Inhibition in Human Models of Synovial Sarcoma.

Sample Metadata Fields

Subject

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accession-icon SRP183695
a1ACT is essential for survival and early cerebellar programming in a critical neonatal window [RNA-Seq]
  • organism-icon Rattus norvegicus
  • sample-icon 68 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Previous study has shown that alpha1ACT is a transcription factor involved with regulating neuronal gene expression. We performed a time-series RNA-seq study using pc12 cell lines stably expressing pcDNA3-alpha1ACT at 4 time points (6hr, 24hr, 3day, and 10day) to explore the transcriptional profiles that capture transient and prolonged dynamic changes regulated by alpha1ACT during cell cycle and differentiation Overall design: PC12 cell lines expressing pcDNA3 (EV) and expressing pcDNA3-a1ACT at 4 different time points (6h, 24h, 3d, 10d) were analyzed by Agilent Bio-analyzer and submitted to university of Chicago Functional genomic facility for library preparation (TruSeq Stranded Total RNA Library Prep Kit with Ribo-Zero Gold, RS-122-2301) and sequencing on Illumina HiSeq2500 platform, with 3 biological replicates for each condition.

Publication Title

α1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon SRP074198
Gene expression profiling of melanoma cell lines by RNASeq
  • organism-icon Homo sapiens
  • sample-icon 61 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Panel of 53 melanoma cell lines were gene expression profiled by RNA-Seq for molecular classification Overall design: mRNA profiles of 53 melanoma cell lines

Publication Title

Interleukin 32 expression in human melanoma.

Sample Metadata Fields

Disease, Disease stage, Cell line, Subject

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accession-icon GSE12288
Gene expression patterns in peripheral blood correlate with the extent of coronary artery disease
  • organism-icon Homo sapiens
  • sample-icon 222 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene expression profile in circulating leukocytes identifies patients with coronary artery disease

Publication Title

Gene expression patterns in peripheral blood correlate with the extent of coronary artery disease.

Sample Metadata Fields

Sex, Age, Specimen part, Race

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accession-icon SRP168173
PolyA-sequencing in IMR-32 neuroblastoma cells with shRNA mediated depletion of CDK12, CDK13 or GFP.
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed RNA-seq analysis of polA transcripts in IMR-32 cells with shRNA-mediated depletion of CDK12 and CDK13 and GFP as a control Overall design: Expression of polA transcripts in IMR-32 cells with shRNA-mediated depletion of CDK12 and CDK13 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) using 2 different shRNA constructs for each target in duplicate, for a total of 10 individual samples Please note that processed data files were generated from the merged replicates, as indicated in the corresponding sample description field.

Publication Title

CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP168172
PolyA-sequencing in Kelly and Kelly E9R neuroblastoma cells treated with THZ531 or DMSO
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed RNA-seq analsysis of polA transcripts in Kelly and Kelly E9 resistant (E9R) cells treated with THZ531 for 6h and DMSO as a control Overall design: Expression of polA transcripts in Kelly and Kelly E9R cells treated with THZ531 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) in duplicate, for a total of 8 indyvidual samples Please note that the bigWig processed data was generated from both replicates and is linked to the corresponding rep1 (*_1) sample records.

Publication Title

CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP140872
PolyA-sequencing in IMR-32 cells treated with THZ531 or DMSO
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We performed RNA-seq analsysis of polA transcripts in IMR-32 cells treated with THZ531 for 2 and 6h and DMSO as a control Overall design: Expression of polA transcripts in IMR-32 treated with THZ531 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) in duplicate, for a total of 6 individual samples

Publication Title

CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE17718
Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to compare the global programme of gene expression in HTLV-positive, ATL-derived and HTLV-positive in vitro-transformed cell lines with that of uninfected primary CD4 T cells.

Publication Title

Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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