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accession-icon GSE21401
Affymetrix microarray for gene expression patterns influenced by syndecan-1 overexpression in malignant mesothelioma STAV-AB cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We aimed to investigate the function of syndecan-1 in tumor cell adhesion and migration, with special focus on the importance of its distinct protein domains, to better understand the structure-function relationship of syndecan-1 in tumor progression. We utilized two mesenchymal tumor cell lines which were transfected to stably overexpress full-length syndecan-1 or truncated variants: the 78 which lacks the extracellular domain except the DRKE sequence proposed to be essential for oligomerization, the 77 which lacks the whole extracellular domain, and the RMKKK which serves as a nuclear localization signal. Various bioassays for cell adhesion, chemotaxis, random movement and wound healing were studied. Furthermore we performed gene microarray to analyze the global gene expression pattern influenced by syndecan-1.

Publication Title

Novel genes and pathways modulated by syndecan-1: implications for the proliferation and cell-cycle regulation of malignant mesothelioma cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37843
Expression data generated by syndecan-1 silencing in malignant mesothelioma STAV-AB cell line
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The transcriptomic responses of syndecan-1 silencing in a human mesothelioma cell line was followed with microarray analysis. To project the transcriptome analysis on the full-dimensional picture of cellular regulation, we applied a novel method of network enrichment analysis which elucidated signalling relations between differentially expressed genes and pathways acting via various molecular mechanisms.

Publication Title

Novel genes and pathways modulated by syndecan-1: implications for the proliferation and cell-cycle regulation of malignant mesothelioma cells.

Sample Metadata Fields

Cell line

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accession-icon GSE39557
Expression data from genetically engineered mouse models (GEMMs)
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

3 Cell lines from Apc, p53 (AP) GEMMs were compared to 12 cell lines from Apc, Kras, p53 (AKP) GEMMs.

Publication Title

Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation.

Sample Metadata Fields

Sex, Cell line

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accession-icon GSE70433
Gene expression in human or mouse brain with iron loading
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE70430
Substantia nigra (SN) and basal ganglia (BG) gene expression in neurodegenertion with brain iron accumulation (NBIA) cases vs normal controls
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Differential gene expression is assessed in substantia nigra and basal ganglia of neurodegenertion with brain iron accumulation cases (BIA) compared to matched normal controls (c).

Publication Title

Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE11893
AHR Activation by TCDD Downregulates Sox9b Expression Producing Jaw Malformation in Zebrafish Embryos
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation.

Publication Title

Aryl hydrocarbon receptor-mediated down-regulation of sox9b causes jaw malformation in zebrafish embryos.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8379
Stb3 deletion affects gene expression within 10 minutes of glucose addition
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Microarrays were conducted to asses the effect of Stb3 deletion in immediate transcriptional induction in response to glucose

Publication Title

Stb3 binds to ribosomal RNA processing element motifs that control transcriptional responses to growth in Saccharomyces cerevisiae.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9020
Comparative Genomics Identifies Gene Targets for Retinoic Acid in the Embryonic Zebrafish Hearts
  • organism-icon Danio rerio
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Retinoic acid (RA) and 2,3,7,8-tetrachlorodibenzo-p-dioxin activate distinct ligand-dependent transcription factors, and both cause cardiac malformation and heart failure in zebrafish embryos. We hypothesized that they cause this response by hyperactivating a common set of genes critical for heart development. To test this, we used microarrays to measure transcripts changes in hearts isolated from zebrafish embryos 1,2,4 and 12 h after exposure to 1M RA. We used hierarchical clustering to compare the transcriptional responses produced in the embryonic heart by RA and TCDD. We could identify no early responses in common between the two agents. However, at 12 h both treatments produced a dramatic downregulation of a common cluster of cell cycle progression genes, which we term the Cell Cycle Gene Cluster (CCGC). This was associated with a halt in heart growth. These results suggest that RA and TCDD ultimately trigger a common transcriptional response associated with heart failure, but not through the direct activation of a common set of genes. Among the genes rapidly induced by RA was Nr2F5, a member of the COUP-TF family of transcription repressors. We found that induction of Nr2F5 was both necessary and sufficient for the cardiotoxic response to RA.

Publication Title

Comparative genomics identifies genes mediating cardiotoxicity in the embryonic zebrafish heart.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33981
Microarray analysis of 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposed Amputated Adult Zebrafish Heart Ventricles
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

The purpose of this experiment is to understand which transcripts are differentially expressed following exposure to TCDD.

Publication Title

TCDD inhibits heart regeneration in adult zebrafish.

Sample Metadata Fields

Treatment

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accession-icon E-MEXP-758
Transcription profiling time series of zebrafish hearts treated with dioxin (TCDD)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

For analysis of gene expression changes in the zebrafish larvae heart in response to TCDD exposure, three replicate samples of heart tissue were collected at 73, 74, 76 and 84 hours post fertilization from larvae exposed to 1 ng/ml TCDD or vehicle from 72 - 73 hours post fertilization. For analysis of gene expression changes in the extracardiac tissue in response to TCDD exposure, three replicate samples of zebrafish larvae bodies with the heart tissue removed were collected at 73, 74, 76 and 84 hours post fertilization from larvae exposed to 1 ng/ml TCDD or vehicle from 72 - 73 hours post fertilization.

Publication Title

Aryl hydrocarbon receptor activation produces heart-specific transcriptional and toxic responses in developing zebrafish.

Sample Metadata Fields

Age, Specimen part, Compound, Time

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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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Developed by the Childhood Cancer Data Lab

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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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