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accession-icon GSE55588
Identification of activity-induced Npas4-regulated genes in cortical inhibitory and excitatory neurons (array)
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify the activity-induced gene expression programs in inhibitory and excitatory neurons, we analyzed RNA extracted from cultured E14 mouse MGE- and CTX-derived neurons (DIV 10) after these cultures were membrane-depolarized for 0, 1 and 6 hrs with 55mM extracellular KCl. To identify the gene programs regulated in these cells by the activity-induced early-response transcription factor Npas4, we repeated the same experiment in the MGE- and CTX-cultures lacking Npas4 (Npas4-KO).

Publication Title

Npas4 regulates excitatory-inhibitory balance within neural circuits through cell-type-specific gene programs.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE9536
The -Catenin Pathway is Overexpressed in Focal Nodular Hyperplasia but not in Cirrhotic FNH-like Nodules
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Focal nodular hyperplasias (FNHs) are benign liver lesions considered to be a hyperplastic response to increased blood flow in otherwise normal liver. In contrast, FNH-like nodules occur in cirrhotic liver but share similar histopathological features. To better understand the pathophysiology of FNH, we performed a transcriptomic analysis. Methods: Affymetrix and cDNA microarrays were used to compare gene expression in eight FNHs with that in tissue from six normal livers. Selected genes were validated with quantitative RT-PCR in 70 benign liver tumors including adenomas and cirrhotic and FNH-like lesions. Results: Among the deregulated genes in FNHs, 19 were physiologically zonated in the normal liver lobule. All six periveinous genes were up-regulated in FNH, whereas 13 genes normally expressed in the periportal area were down-regulated. Immunohistochemistry revealed that glutamine synthetase was markedly overexpressed, forming anastomosed areas usually centered on visible veins. -catenin mRNA was slightly but significantly overexpressed, as were several known -catenin target genes. Moreover, activated hypophosphorylated -catenin protein accumulated in FNH in the absence of activating mutations. These results suggest zonated activation of the -catenin pathway specifically in FNH, whereas the other benign hepatocellular tumors, including FNH-like lesions, demonstrated an entirely different pattern of -catenin expression. Conclusions: In FNH, increased expression of the -catenin pathway was restricted to enlarged periveinous areas, which may explain the slight polyclonal over-proliferation of hepatocytes at the origin of the lesion. FNH-like nodules may have a different pathogenetic origin.

Publication Title

The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE11819
Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Inflammatory hepatocellular adenomas (IHCA) are benign liver tumours defined by the presence of inflammatory infiltrates and by the elevated expression of inflammatory proteins in tumour hepatocytes1,2. Here we show a striking activation of the IL6 signalling pathway in this tumour type, and sequencing candidate genes pinpointed this response to somatic gain-of-function mutations in the IL6ST gene that encodes the signalling co-receptor gp130. Indeed, ~70% of IHCA harbour small in-frame deletions that target the binding site of gp130 for IL6, and expression of the most frequent gp130 mutant, Delta-STVY190, in hepatocellular cells activates STAT3 in absence of ligand. Further, analysis of hepatocellular carcinomas revealed rare gp130 alterations always accompanied by -catenin-activating mutations, suggesting a cooperative effect of these signalling pathways in the malignant conversion of hepatocytes. The recurrent gain-of-function gp130 mutations in these human hepatocellular adenomas explains their inflammatory phenotype, and suggest that similar alterations may occur in other inflammatory epithelial tumours with STAT3 activation.

Publication Title

Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE60049
Gene expression data from cultured mouse cortical (mCTX) neurons in different stimulation and knockdown conditions
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Although the induction of C-FOS in the brain has been extensively studied for several decades to date there has been no attempt to identify the targets of C-FOS at a genome wide level, and it was not known how many genes C-FOS activates in a given cell. To identify potential C-FOS target genes, we performed microarray analysis on RNA obtained from mouse cortical (mCTX) neurons infected with lentivirus containing either a control shRNA (targeting firefly luciferase) or c-Fos shRNA that were subsequently depolarized with 0, 1, 3, or 6 hours of KCl.

Publication Title

Genome-wide identification and characterization of functional neuronal activity-dependent enhancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE48024
Time series of global gene expression after trivalent influenza vaccination in humans
  • organism-icon Homo sapiens
  • sample-icon 519 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative genomic analysis of the human immune response to influenza vaccination.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject, Time

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accession-icon GSE48018
Time series of global gene expression after trivalent influenza vaccination in humans (male cohort)
  • organism-icon Homo sapiens
  • sample-icon 431 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

The purpose of the study was to assess the patterns of global gene expression in peripheral blood cells before and at three time points after the administration of a trivalent influenza vaccine in human male subjects, and to relate these to the antibody response to the vaccine. The antibody titer data for these subjects is provided as a supplemental file.

Publication Title

Integrative genomic analysis of the human immune response to influenza vaccination.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject, Time

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accession-icon GSE48023
Time series of global gene expression after trivalent influenza vaccination in humans (female cohort)
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

The purpose of the study was to assess the patterns of global gene expression in peripheral blood cells before and at three time points after the administration of a trivalent influenza vaccine in human female subjects, and to relate these to the antibody response to the vaccine

Publication Title

Integrative genomic analysis of the human immune response to influenza vaccination.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject, Time

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accession-icon GSE11704
Absence of host innate immune responses in SARS-CoV-infected ferrets upon subsequent challenge
  • organism-icon Mustela putorius furo
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Canine Genome 2.0 Array (canine2)

Description

To further investigate the underlying mechanisms of severe acute respiratory syndrome (SARS) pathogenesis and evaluate the therapeutic efficacy of potential drugs and vaccines it is necessary to use an animal model that is highly representative of the human condition in terms of respiratory anatomy, physiology and clinical sequelae. The ferret, Mustela putorius furo, supports SARS-CoV replication and displays many of the symptoms and pathological features seen in SARS-CoV-infected humans. We have recently established a SARS-CoV infection-challenge ferret platform for use in evaluating potential therapeutics to treat SARS. The main objective of the current study was to extend our previous results and identify early host immune responses upon infection and determine immune correlates of protection upon challenge with SARS-CoV in ferrets.

Publication Title

Lack of innate interferon responses during SARS coronavirus infection in a vaccination and reinfection ferret model.

Sample Metadata Fields

Specimen part

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accession-icon GSE62232
Large-scale gene expression profiling of 81 hepatocellular carcinomas
  • organism-icon Homo sapiens
  • sample-icon 90 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatocellular carcinoma (HCC) is ranked second in cancer-associated deaths worldwide. Most cases of HCC are secondary to either a viral hepatitis infection (hepatitis B or C) or cirrhosis (alcoholism being the most common cause of hepatic cirrhosis). It is a complex and heterogeneous tumor due to activation of multiple cellular pathways and molecular alterations.

Publication Title

Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE137773
An in vivo systematic genetic analysis of tumour progression in Drosophila identifies the cohesin complex as an invasion suppressor
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Metastasis is the leading cause of death for cancer patients. Consequently it is imperative that we improve our understanding of the molecular mechanisms that underlie progression of tumour growth towards malignancy. Advances in genome characterisation technologies have been very successful in identifying commonly mutated or misregulated genes in a variety of human cancers. However the difficulty in evaluating whether these candidate genes drive tumour progression remains a major challenge. Using the genetic amenability of Drosophila melanogaster we generated tumours with specific genotypes in the living animal and carried out a detailed systematic loss-of-function analysis to identify conserved genes that enhance or suppress epithelial tumour progression. This enabled the discovery of functional cooperative regulators of invasion and the establishment of a network of conserved invasion suppressors. This includes constituents of the cohesin complex, which can either promote individual or collective invasion, depending on the severity of effect on cohesin function.

Publication Title

A Genetic Analysis of Tumor Progression in Drosophila Identifies the Cohesin Complex as a Suppressor of Individual and Collective Cell Invasion.

Sample Metadata Fields

Cell line

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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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