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accession-icon GSE90580
Gene expression profiles of pre-confluent 3T3-L1 preadipocytes with low or high adipogenic potential
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The objective of this analysis was to identify the genes that are differentially expressed between preadipocytes with low or high adipogenic capability

Publication Title

Amplification of Adipogenic Commitment by VSTM2A.

Sample Metadata Fields

Specimen part

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accession-icon GSE10798
Transcriptional analysis of the sweet orange interaction with the citrus canker pathogens
  • organism-icon Citrus sinensis
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Citrus Genome Array (citrus)

Description

We have used the citrus GeneChip array (GPL5731) to survey the transcription profiles of sweet orange in response to the bacterial pathogens Xanthomonas axonopodis pv. citri (Xac) and Xanthomonas axonopodis pv. aurantifolii (Xaa). Xac is the causal agent of the citrus canker disease on a wide range of citrus species, including sweet oranges (Citrus sinensis). On the other hand, Xaa is pathogenic to Mexican lime (Citrus aurantifolia) only, and in sweet orange it triggers a defense response. In order to identify the genes induced during the defense response (Xaa-responsive genes) or citrus canker development (Xac-responsive genes), we conducted microarrays hybridization experiments at 6 and 48 hours after bacterial infiltration (habi). The analysis revealed that genes commonly modulated by Xac and Xaa are associated with basal defenses normally triggered by pathogen-associated molecular patterns, including those involved in reactive oxygen species production and lignification. Significantly, Xac-infected leaves showed considerable changes in the transcriptional profiles of defense-, cell wall-, vesicle trafficking- and cell growth-related genes between 6 and 48 habi. This is consistent with the notion that Xac suppresses host defenses near the beginning of the infection and simultaneously changes the physiological status of the host to promote cell enlargement and division. Finally, Xaa triggered a MAP kinase signaling pathway involving WRKY and ethylene-responsive transcriptional factors known to activate downstream defense genes.

Publication Title

Transcriptional analysis of the sweet orange interaction with the citrus canker pathogens Xanthomonas axonopodis pv. citri and Xanthomonas axonopodis pv. aurantifolii.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41909
IL-7 and IL-15 instruct the generation of human memory stem T cells from nave precursors
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The identification of the most appropriate T-cell subset to ensure optimal persistence and anti-tumor activity is a major goal of cancer immunotherapy. We identified a novel post-mitotic CD45RA+CD62L+ T cell subpopulation (TTN), generated in vitro upon activation of nave T (TN) cells with beads conjugated to anti-CD3 and anti-CD28 antibodies. This cell population is highly proliferative, produces low levels of IFNg and cytotoxic molecules, and requires IL-7 and IL-15 for in vitro expansion.

Publication Title

IL-7 and IL-15 instruct the generation of human memory stem T cells from naive precursors.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28997
Function-based discovery of significant transcriptional temporal patterns in insulin-stimulated muscle cells
  • organism-icon Rattus norvegicus
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Background: Insulin's effect on protein synthesis (translation of transcripts) and post-translational modifications, especially those involving reversible modifications such as phosphorylation of various signaling proteins, are extensively studied. On the other hand, insulin's effect on the transcription of genes, especially of transcriptional temporal patterns, is not well investigated in the literature.

Publication Title

Function-based discovery of significant transcriptional temporal patterns in insulin stimulated muscle cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE12205
Effect of PTP inhibition on changes in gene expression after Cr(VI) exposure
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although the consequences of genotoxic injury include cell cycle arrest and apoptosis, cell survival responses after genotoxic injury can produce intrinsic death-resistance and contribute to the development of a transformed phenotype. Protein tyrosine phosphatases (PTPs) are integral components of key survival pathways, and are responsible for their inactivation, while PTP inhibition is are often associated with enhanced cell proliferation. Our aim was to elucidate signaling events that modulate cell survival after genotoxin exposure. Diploid human lung fibroblasts (HLF) were treated with Cr(VI) (as Na2CrO4), a well known human respiratory carcinogen that induces a wide spectrum of DNA damage, in the presence and absence of a broad-range PTP inhibitor, sodium orthovanadate. Notably, PTP inhibition abrogated Cr(VI)-induced clonogenic lethality. The enhanced survival of Cr(VI)-exposed cells after PTP inhibition was predominantly due to a bypass of cell cycle arrest and was not due to decreased Cr uptake as evidenced by unchanged Cr-DNA adduct burden. Additionally, the bypass of Cr-induced growth arrest by PTP inhibition, was accompanied by a decrease in Cr(VI)-induced expression of cell cycle inhibiting genes, and an increase in the Cr(VI)-induced expression of cell cycle promoting genes. Importantly, PTP inhibition resulted in an increase in forward mutations at the HPRT locus, supporting the hypothesis that PTP inhibition in the presence of DNA damage may lead to genomic instability, via bypass of cell cycle checkpoints.

Publication Title

Bypass of hexavalent chromium-induced growth arrest by a protein tyrosine phosphatase inhibitor: enhanced survival and mutagenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE48964
Expression data from Adipose Stem Cells (ASC) from morbidly obese and non-obese individuals
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The adipose tissue is an endocrine regulator and a risk factor for atherosclerosis and cardiovascular disease when by excessive accumulation induces obesity. Although the adipose tissue is also a reservoir for stem cells (ASC) their function and stemcellness has been questioned. Our aim was to investigate the mechanisms by which obesity affects subcutaneous white adipose tissue (WAT) stem cells.

Publication Title

Stem cells isolated from adipose tissue of obese patients show changes in their transcriptomic profile that indicate loss in stemcellness and increased commitment to an adipocyte-like phenotype.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041263
RUNX3 Facilitates Growth of Ewing Sarcoma Cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. Overall design: RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA

Publication Title

RUNX3 facilitates growth of Ewing sarcoma cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE58812
Gene-expression molecular subtyping of triple-negative breast cancer tumours: importance of immune response
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Triple-negative (TN) breast cancers need to be refined in order to identify therapeutic subgroups of patients.

Publication Title

Gene-expression molecular subtyping of triple-negative breast cancer tumours: importance of immune response.

Sample Metadata Fields

Disease

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accession-icon GSE10445
MERLION LUNG CANCER STUDY
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Series of stage IB lung adenocarcinomas and large cell carcinomas. The aim of the study was to predict outcome using a Copy Number Driven Gene Expression signature.

Publication Title

Prediction of clinical outcome in multiple lung cancer cohorts by integrative genomics: implications for chemotherapy selection.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065032
Genetic and Acquired Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration
  • organism-icon Danio rerio
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

A zebrafish forward genetic screen for determinants of susceptibility to Mycobacterium marinum identified a hypersusceptible mutant deficient in the lysosomal hydrolase Cathepsin L that manifests the hallmarks of human lysosomal storage diseases. In uninfected mutants, macrophages progressively accumulate undigested material in their lysosomes, leading to impaired migration and the accumulation of unengulfed cell debris. During mycobacterial infection, these vacuolated macrophages cannot migrate to phagocytose infected macrophages undergoing apoptosis in the tuberculous granuloma. Consequently, unengulfed apoptotic macrophages undergo secondary necrosis causing granuloma breakdown and increased mycobacterial growth. Macrophage lysosomal accumulations similarly impair migration to newly infecting mycobacteria. We find that important aspects of this phenotype are recapitulated in human smokers, who are at increased risk for tuberculosis. A majority of alveolar macrophages from smokers exhibit lysosomal accumulations and do not migrate to Mycobacterium tuberculosis. This incapacitation of highly microbicidal first-responding macrophages may contribute to smokers' susceptibility to tuberculosis. Overall design: A forward genetic screen for zebrafish larvae that are hypersusceptible to Mycobacterium marinum infection identified a mutation in the transcription factor snapc1b at 13: 37996163 (T->C). Individuals of wild type (T/T) and mutant (C/C) were genotyped and pooled respectively for RNA isolation and transcriptome analysis.

Publication Title

Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration.

Sample Metadata Fields

No sample metadata fields

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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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