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accession-icon GSE25828
Pten deficiency cooperates with KrasG12D to activate NFkB pathway promoting the development of malignant pancreatic ductal adenocarcinoma
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Almost all human pancreatic ductal adenocarcinomas (PDACs) are driven by oncogenic Kras and the progression of the disease is characterized by the serial appearance of certain genetic lesions. Mouse models have convincingly shown that Kras mutation induces classical PanIN lesions that can progress to PDAC in the appropriate tumor suppressor background. However, the cooperative mechanism between mutant Kras-dependent signaling surrogates and other oncogenic pathways remains to be fully elucidated in order to devise better therapeutic strategy. Mounting evidence PTEN/PI3K perturbation on PDAC tumorigenesis, we observed frequent PTEN inactivation at both genomic and histopathological levels in primary human PDAC samples. The importance of PTEN/PI3K pathway during the development of PDAC was further supported by genetic studies demonstrating that Pten deficiency in cooperation with Kras activation accelerated the formation of invasive PDAC. Mechanistically, combined Kras mutation and Pten inactivation leads to NFkB activation and subsequent induction of cytokine pathways, accompanied with strong stromal activation and immune cell infiltration. Therefore, PTEN/PI3K pathway dictates the activity of NFkB network and serves as a major surrogate during Kras-mediated pancreatic tumorigenesis.

Publication Title

PTEN is a major tumor suppressor in pancreatic ductal adenocarcinoma and regulates an NF-κB-cytokine network.

Sample Metadata Fields

Specimen part

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accession-icon GSE48383
ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Combinatorial recruitment of CREB, C/EBPβ and c-Jun determines activation of promoters upon keratinocyte differentiation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE48382
ChIp-Chip using RNAP II, CREB C/EBPb and cJun antibody in undifferentiated or differentiated keratinocytes (expression)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Combinatorial recruitment of CREB, C/EBPb and Jun determines activation of promoters upon keratinocyte differentiation

Publication Title

Combinatorial recruitment of CREB, C/EBPβ and c-Jun determines activation of promoters upon keratinocyte differentiation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE29983
Comparison of gene expression profiles for hormone induction in the presence and absence of AP1 binding.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Gene expression array analysis component. Ligand-dependent transcription by the nuclear receptor glucocorticoid receptor (GR) is mediated by interactions with co-regulators. The role of these interactions in determining selective binding of GR to regulatory elements remains unclear. Recent findings indicate a large fraction of genomic GR binding coincides with chromatin that is accessible prior to hormone treatment, suggesting that receptor binding is dictated by proteins that maintain chromatin in an open state. Combining nucleolytic cleavage and chromatin immunoprecipitation with high-throughput sequencing, we identify the activator protein 1 (AP1) as a major partner for productive GR-chromatin interactions. AP1 is critical for GR-regulated transcription and recruitment to co-occupied regulatory elements, illustrating an extensive AP1-GR interaction network. Importantly, the maintenance of baseline chromatin accessibility facilitates GR recruitment and is dependent on AP1 binding. We propose a model where the basal occupancy of transcription factors act to prime chromatin and direct inducible transcription factors to select regions in the genome.

Publication Title

Transcription factor AP1 potentiates chromatin accessibility and glucocorticoid receptor binding.

Sample Metadata Fields

Sex, Cell line, Treatment, Time

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accession-icon GSE3368
Genomic Analysis of the Xenopus Organizer
  • organism-icon Xenopus laevis
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Studies of the Xenopus organizer have laid the foundation for our understanding of the conserved signaling pathways that pattern vertebrate embryos during gastrulation. Here, we use this wealth of knowledge as leverage in the design and analysis of a genomic visualization of organizer-related gene transcription. Using ectopic expression of the two major activities of the organizer, BMP and Wnt inhibition, as well as endogenous tissues, we generate a focused set of samples that represent different aspects of organizer signaling. The genomic expression values of each sample are then measured with oligonucleotide arrays. From this data, genes regulated by organizer signaling are selected and then clustered by their patterns of regulation. A new GO biological process annotation of the Xenopus genome allows us to rapidly identify clusters that are highly enriched for known gastrula patterning genes. Within these clusters, we can predict the expression patterns of unknown genes with remarkable accuracy, leading to the discovery of new organizer-related gastrula stage expression patterns for 19 genes. Moreover, the patterns of gene response observed within these clusters allow us to parse apart the contributions of BMP and Wnt inhibition in organizer function. We find that the majority of gastrula patterning genes respond transcriptionally to these activities according to only a few stereotyped patterns, allowing us to describe suites of genes that are likely to share similar regulatory mechanisms. These suites of genes demonstrate a mechanism where BMP inhibition initiates the organizer program before gastrulation, and Wnt inhibition maintains and drives the organizer program during gastrulation.

Publication Title

Genomic analysis of Xenopus organizer function.

Sample Metadata Fields

Specimen part

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accession-icon GSE28795
Expression data from E. coli cells overexpressing either GreA or GreB in ppGpp0 cells in the dksA+ or dksA- background
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Strains devoid of ppGpp (relA spoT; called ppGpp0), and ppGpp0 dksA- exhibit several amino acid requirements for growth on minimal media. We found that overexpression of DksA can complement some of those requirements. Since DksA is a factor that binds to the RNA polymerase secondary channel, we wondered if other secondary channel proteins might also exert a similar role with respect to growth on minimal media. In our study we found that GreA and partially GreB can in fact complement these requirements under certain conditions. Here, we wished to investigate a broader effect of GreA and GreB on ppGpp0 and ppGpp0 dksA- strains. Since the parent strains are unable to grow in minimal media, we had to supplement the M9 glucose medium with a set of amino acids (DFHILQSTV). We found that both, GreA and GreB can affect a much larger set of genes in the absence of dksA, than in its presence. Also, GreA seems to affect more genes than GreB, under both conditions.

Publication Title

Effects on growth by changes of the balance between GreA, GreB, and DksA suggest mutual competition and functional redundancy in Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE152494
Robustness testing and optimization of an adverse outcome pathway on cholestatic liver injury
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to provide a transcriptomic signature of different types of cholestasis evoked by 3 different drugs and obstructive surgery

Publication Title

Robustness testing and optimization of an adverse outcome pathway on cholestatic liver injury.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE48406
Maize gene expression during infection with the Ustilago maydis mutant for cluster 19A and subdeletions for individual genes of cluster 19A
  • organism-icon Zea mays
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Maize Genome Array (maize)

Description

Many of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets. Many of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets.

Publication Title

Characterization of the largest effector gene cluster of Ustilago maydis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE37263
Genome-wide profiling of altered gene expression in the neocortex of Alzheimer's disease (gene level)
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

We investigated genome-wide gene alterations in the temporal cortex of a well-characterized cohort of Alzheimers disease (AD) patients using Affymetrix exon arrays.

Publication Title

Genome wide profiling of altered gene expression in the neocortex of Alzheimer's disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE73817
Expression data from leaves of Hordeum vulgare at seedling stage
  • organism-icon Hordeum vulgare
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

A DNA microarray analysis detected large-scale changes of gene expression in response to Cd stress with a substantial difference between the two barley genotypes differing in Cd tolerance and accumulation. Cd stress led to higher expression of genes involved in transport, carbohydrate metabolism and signal transduction in the low-grain-Cd-accumulating genotype. Novel transporter genes such as zinc transporter genes were identified as being associated with low Cd accumulation.

Publication Title

DNA microarray revealed and RNAi plants confirmed key genes conferring low Cd accumulation in barley grains.

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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